ยืดอายุให้ยืนยาวด้วย ‘ทูน่า’

bangkokbiznews140307_001โรคหัวใจและหลอดเลือดเป็นปัญหาสุขภาพที่มีแนวโน้มสูงขึ้นทุกปี จากข้อมูลของสำนักงานหลักประกันสุขภาพแห่งชาติ (สปสช.) ในปี 2556 พบว่า โรคหัวใจเป็นโรคที่มีอัตราการเสียชีวิตติดอันดับ 1 ใน 10 ของโรคที่มีอัตราการตายสูงสุดในประเทศไทย และยังส่งผลให้เกิดความสูญเสียทางเศรษฐกิจถึงปีละประมาณ 50,000 ล้านบาท จากการวิจัยและคำแนะนำของแพทย์เพื่อยืดอายุให้ยืนยาวพร้อมกับลดความเสี่ยงจากโรคหัวใจนั้นสามารถเริ่มต้นง่ายๆ ด้วยการรับประทานปลา โดยเฉพาะปลาทะเลน้ำลึกที่อุดมไปด้วยกรดไขมันโอเมก้า 3 ที่เต็มเปี่ยมด้วยคุณค่าทางโภชนาการและมากประโยชน์ต่อสุขภาพ

กรดไขมันโอเมก้า 3 เป็นกรดไขมันไม่อิ่มตัวที่ร่างกายสร้างเองไม่ได้ จำเป็นต้องได้รับจากอาหาร ซึ่งพบได้มากในปลาทะเลน้ำลึกทั้งในปลาแซลมอน ปลาซาร์ดีน ปลาแมคเคอเรล และปลาทูน่า ที่มีไขมัน โอเมก้า 3 สูงถึง 1 – 4 กรัม ต่อเนื้อปลา 100 กรัม กรดไขมันโอเมก้า 3 ที่สำคัญมี 2 ชนิด ได้แก่ EPA (EICOSAPENTAENOIC ACID) และ DHA (DOCOSAHEXAENOIC ACID) ที่เป็นประโยชน์ต่อผู้สูงอายุ ซึ่งจะช่วยลดความเสี่ยงของการเกิดโรคหลอดเลือดหัวใจได้ เนื่องจากโอเมก้าไปช่วยลดการเกาะตัวของเกล็ดเลือดและการหดตัวของหลอดเลือด จึงส่งผลให้เกิดลิ่มเลือดอุดตันได้ยากขึ้น อีกทั้งยังช่วยลดอัตราเสี่ยงโรคหัวใจล้มเหลว และช่วยลดระดับไขมันไตรกลีเซอไรด์ในเลือดจึงลดความเสี่ยงการเกิดโรคหลอดเลือดได้

ผลการศึกษาวิจัยของนักวิทยาศาสตร์จากคณะสาธารณสุขมหาวิทยาลัยฮาร์วาร์ดในสหรัฐ พบว่าผู้ใหญ่อายุ 65 ปีขึ้นไปที่กินปลาเป็นประจำมีโอเมก้า 3 ในปริมาณสูง ทำให้มีอายุเฉลี่ยยืนยาวมากกว่าผู้ที่ไม่บริโภคกรดไขมันโอเมก้า 3 ถึง 2 ปี ทั้งนี้ พบความเชื่อมโยงว่าผู้ที่มีระดับโอเมก้า 3 ในร่างกายในปริมาณสูงมีความเสี่ยงเสียชีวิตด้วยโรคหัวใจเพียงร้อยละ 35 น้อยกว่าผู้มีระดับความดันโลหิตต่ำ นอกจากนั้นทางสมาคมแพทย์โรคหัวใจอเมริกันยังแนะนำเพิ่มเติมว่าวิธีที่ดีที่สุดในการเพิ่มกรดโอเมก้า 3 ในร่างกาย คือ เพิ่มการรับประทานปลาทะเลสัปดาห์ละ 2-3 ครั้ง เพื่อช่วยลดความเสี่ยงโรคหัวใจและหลอดเลือด

ที่มา : กรุงเทพธุรกิจ 7 มีนาคม 2557

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Credit: better4you.mbooth.com

Credit: better4you.mbooth.com

Ask the Expert: Omega-3 Fatty Acids

The Expert

Dr. Frank Sacks

Professor of Cardiovascular Disease Prevention, Department of Nutrition, Harvard School of Public Health

1. What are omega-3 fatty acids, and why should I make sure to include them in my diet?

Omega-3 fatty acids (also known as n-3 fatty acids) are polyunsaturated fatty acids that are essential nutrients for health. We need omega-3 fatty acids for numerous normal body functions, such as controlling blood clotting and building cell membranes in the brain, and since our bodies cannot make omega-3 fats, we must get them through food. Omega-3 fatty acids are also associated with many health benefits, including protection against heart disease and possibly stroke. New studies are identifying potential benefits for a wide range of conditions including cancer, inflammatory bowel disease, and other autoimmune diseases such as lupus and rheumatoid arthritis.

2. What foods are good sources of omega-3 fatty acids? How much do I need to eat of these foods to get enough omega-3s?

There are two major types of omega-3 fatty acids in our diets: One type is alpha-linolenic acid (ALA), which is found in some vegetable oils, such as soybean, rapeseed (canola), and flaxseed, and in walnuts. ALA is also found in some green vegetables, such as Brussels sprouts, kale, spinach, and salad greens. The other type, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), is found in fatty fish. The body partially converts ALA to EPA and DHA.

We do not know whether vegetable or fish omega-3 fatty acids are equally beneficial, although both seem to be beneficial. Unfortunately, most Americans do not get enough of either type. For good health, you should aim to get at least one rich source of omega-3 fatty acids in your diet every day. This could be through a serving of fatty fish (such as salmon), a tablespoon of canola or soybean oil in salad dressing or in cooking, or a handful of walnuts or ground flaxseed mixed into your morning oatmeal.

3. What are omega-6 fatty acids? Should I be concerned about the ratio of omega-6 fatty acids to omega-3 fatty acids in my diet?

Omega-6 fatty acids (also known as n-6 fatty acids) are also polyunsaturated fatty acids that are essential nutrients, meaning that our bodies cannot make them and we must obtain them from food. They are abundant in the Western diet; common sources include safflower, corn, cottonseed, and soybean oils.

Omega-6 fatty acids lower LDL cholesterol (the “bad” cholesterol) and reduce inflammation, and they are protective against heart disease. So both omega-6 and omega-3 fatty acids are healthy. While there is a theory that omega-3 fatty acids are better for our health than omega-6 fatty acids, this is not supported by the latest evidence. Thus the omega-3 to omega-6 ratio is basically the “good divided by the good,” so it is of no value in evaluating diet quality or predicting disease.

4. Is it better to get omega-3 fatty acids from food or from supplements?

Certainly foods, since the plants and fish that contain omega-3 fats have other good nutrients, such as protein, vitamins and minerals. People who do not eat fish or other foods rich in omega-3 fatty acids should consider taking an omega-3 supplement of 500 mg per day; fish oil is used in supplements, but there are also vegetarian supplements that have ALA. Studies suggest that people who have already had a heart attack may benefit from higher doses of omega-3 supplements (basically, double the 500 mg), so if you do have heart disease, consult your healthcare provider about whether taking a higher dose of omega 3s makes sense for you.

5. I am a vegetarian, so I do not consume any fish. But I get plenty of ALA in my diet, from canola and soybean oil, ground flax seed, and walnuts. How efficiently does the body convert ALA to DHA and EPA? Should I take an algal DHA supplement?

If you are getting adequate ALA in your diet from oils and nuts, I am not sure you really need to take an algal DHA supplement. As I mentioned above, the body partially converts ALA to EPA and DHA; it is not known if ALA has substantial health benefits as is, or whether it must be converted to EPA and DHA to produce most of the benefits. My current interpretation of the science is that ALA is important to nutrition because it is an essential fatty acid, and that at least part of its benefits come from its conversion to EPA and DHA. I don’t advocate that vegans take n-3 supplements if they are getting ALA from vegetable oils, vegetables, walnuts, and other vegetarian sources as described above.

6. Can omega-3 fatty acids be destroyed by high-heat cooking?

Not if the oil is fresh. In fact, even in frying oil that is used for days, you still can find ALA in it.

SOURCE : www.hsph.harvard.edu

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นักวิจัยอเมริกันชี้ว่าเกลือในอาหารมีผลให้เกิดโรคแพ้ภูมิตนเอง

voathai130320_001ทีมนักวิทยาศาสตร์อเมริกันหลายทีมพบว่าเกลือที่ผสมในอาหารมีผลให้เกิดกลุ่มโรคแพ้ภูมิตนเองหรือกลุ่มโรคออโต้อิมมูน เป็นอาการที่เกิดจากระบบภูมิต้านทานของร่างกายไปต่อต้านและทำลายเนื้อเยื่อที่เเข็งแรงในร่างกายและอวัยวะต่างๆ

นักวิทยาศาสตร์สามารถระบุยีนที่มีความแตกต่างจากยีนปกติได้ราวหนึ่งร้อยตัว ที่ปรับเปลี่ยนไปจากเดิมหลังจากสลับโมเลกุลของยีนภายในเซลล์ของสิ่งมีชีวิต โดยเชื่อว่ายีนที่แตกต่างจากยีนปกติเหล่านี้น่าจะมีส่วนก่อให้เกิดกลุ่มโรคแพ้ภูมิตนเอง รวมทั้งโรคปลอกประสาทอักเสบ หรือโรคมัลติเพิล สเคลอโรซีส (Multiple Sclerosis) ที่เรียกสั้นๆว่าเอ็มเอส (MS)

นักวิทยาศาสตร์พบหลักฐานยืนยันว่าการปรับเปลี่ยนลักษณะของยีนเหล่านี้ไม่สืบทอดมาจากพันธุกรรมพ่อแม่แต่น่าจะเกิดจากปัจจุยกระตุ้นจากสภาพแวดล้อมภายนอก ผู้เชี่ยวชาญเชื่อว่าสาเหตุที่กระตุ้นให้เกิดโรคภูมิต้านตนเองอาจมาจากการติดเชื้อ การขาดวิตามินดี การสูบบุหรี่และความอ้วน การวิจัยชิ้นล่าสุดในเรื่องนี้พบว่าเกลือที่ผสมในอาหารรับประทานอาจเป็นปัจจัยที่กระตุ้นให้ยีนเกิดการเปลี่ยนแปลงในเซลล์ทำให้ภูมิต้านทานเกิดความสับสนและหันไปทำลายเนื่อเยื่อที่แข็งแรงแทนที่จะไปทำลายเชื้อโรคและสิ่งแปลกปลอมที่เข้าสู่ร่างกาย

ในรายงานผลการวิจัยอย่างน้อยสองชิ้นที่เพิ่งตีพิมพ์ไปเมื่อเร็วๆนี้ ทีมนักวิทยาศาสตร์ที่มหาวิทยาลัย Harvard Medical School และที่สถาบัน Broad Insitute ในรัฐ Massachusetts อธิบายลักษณะความเป็นไปได้ของการเปลี่ยนแปลงทางโมเลกุลในยีนในหลายลักษณะที่เกิดจากอาการภูมิต้านอันเกิดจากการบริโภคเกลือ

และในผลการศึกษาชิ้นที่สาม ทีมนักวิจัยที่มหาวิทยาลัยเยลเปิดเผยผลการทดลองผลกระทบของเกลือต่อร่างกายหนูทดลอง โดยนักวิจัยแบ่งกลุ่มหนูทดลองเป็นสองกลุ่ม กลุ่มแรกเลี้ยงด้วยอาหารที่มีเกลือผสมอยู่ในปริมาณต่ำ กลุ่มที่สองเลี้ยงด้วยอาหารที่มีเกลือผสมอยู่ในปริมาณสูง แต่หนูทดลองทั้งหมดได้รับการเพาะพันธุ์ให้พัฒนาโรคที่คล้ายกับโรคปลอกประสาทอักเสบหรือเอ็มเอส

คุณเดวิด ฮัฟเฟล่อ หัวหน้าแผนกประสาทวิทยาที่มหาวิทยาลัยเลย กล่าวว่าหนูทดลองที่กินเกลือเข้าไปในปริมาณน้อยกว่ายังเดินได้ดีแต่ควบคุมการทำงานของหางไม่ได้ดีเท่าที่ควร

คุณฮัฟเล่อร์ หัวหน้าทีมวิจัยกล่าวกับผู้สื่อข่าววีโอเอว่าหนูทดลองที่ได้รับเกลือในปริมาณสูงกลายเป็นอัมพาต ไม่สามารถเคลื่อนไหวไปรอบๆกรงได้ เขาคิดว่าผลการทดลองสร้างภาพที่ชัดเจนถึงผลกระทบของเกลือต่อการกำเริบของโรคปลอกประสาทอักเสบในหนูทดลอง

คุณฮัฟเล่อร์กล่าวว่าทีมนักวิจัยของเขาพบหลักฐานความเกี่ยวโยงนี้โดยบังเอิญ ขณะทำการศึกษาชนิดของเชื้อเเบคทีเรียหลายพันธุ์ที่อาศัยอยู่ในลำใส้ของคนอย่างน้อยหนึ่งร้อยตัวอย่าง นักวิจัยพบว่าคนที่บริโภคอาหารฟ้าสฟู้ดมีปริมาณทีเซลล์ที่เเสดงว่ามีอาการอักเสบในกระแสเลือดสูง อาการอักเสบดังกล่าวเป็นสัณญาณว่าระบบภูมิต้านทานเริ่มต้นทำงานแล้ว กลุ่มโรคภูมิต้านตนเองนี้รวมทั้งโรคเอ็มเอส เบาหวานประเภทที่หนึ่ง ลูปุส โรครูมาตอยด์ มีคนป่วยด้วยโรคเหล่านี้เพิ่มมากขึ้นในปัจจุบัน แม้แต่อัตราการเกิดโรคหัวใจ ที่เกิดจากการทำงานผิดพลาดของระบบภูมิต้านทานนี้ก็เิ่พิ่ม ขึ้นอย่างมาก และผลการศึกษาได้เเสดงให้เห็นว่าเกลืออาจจะเป็นปัจจัยทางสิ่งแวดล้อมที่ก่อให้เกิดกลุ่มโรคเหล่านี้ ซึ่งเป็นการค้นพบที่ใหม่ที่ไม่มีใครรู้มาก่อนหน้านี้

Jessica Berman
20.03.2013

ที่มา : www.voathai.com

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foxnews130307_001

Too much salt may trigger autoimmune diseases, studies find

Published March 07, 2013
Reuters

Increased salt consumption may be a key culprit behind rising rates of autoimmune diseases such as multiple sclerosis, researchers reported on Wednesday in a trio of papers looking at the role of a specific class of cells linked with inflammation.

Reporting in the journal Nature, the researchers said high-salt diets increased levels of a type of immune cell linked with autoimmune disease. And mice genetically engineered to develop multiple sclerosis (MS) got much worse when they ate what amounted to a high-salt Western diet compared with mice who had more moderate salt intake.

The findings suggest that salt may play a previously unknown role in triggering autoimmune diseases such as MS or type 1 diabetes in individuals who are already genetically predisposed.

“It’s not bad genes. It’s not bad environment. It’s a bad interaction between genes and the environment,” said Dr. David Hafler, a professor of immunobiology at Yale University in New Haven, Connecticut, and senior author of one of the three papers.

High salt intake is already a known culprit in increasing the risk of heart disease and hypertension. The new study now implicates high-salt diets in increasing rates of autoimmune disease. “It can’t be just salt. We know vitamin D probably plays a small component. We know smoking is a risk factor. This now suggests that salt is also a risk factor,” Hafler said.

“How much? We don’t know,” he added.

Hafler became interested in studying the link between salt and autoimmunity through studies of the gut microbiome – a census of gut microbes and cell function of 100 healthy individuals.

The team noticed that when people in the study visited fast food restaurants more than once a week, they saw a marked increase in levels of destructive inflammatory cells, which the immune system produces to respond to injury or foreign invaders, but which attack healthy tissues in autoimmune diseases.

He shared these findings with colleagues at Harvard Medical School and the Broad Institute of Harvard and the Massachusetts Institute of Technology and others who were working out what factors induce the activity of a type of autoimmune cell known as a T helper 17 or a Th17 cell.

Th17 cells can promote inflammation that is important for defending against pathogens, but they have also been linked to diseases like multiple sclerosis, psoriasis, rheumatoid arthritis, and ankylosing spondylitis. Treatment options for some of these diseases, such as psoriasis, include manipulating T cell function.

“The question we wanted to pursue was: How does this highly pathogenic, pro-inflammatory T cell develop?” said Vijay Kuchroo of the Harvard-affiliated Brigham and Women’s Hospital and a member of the Broad Institute.

“Once we have a more nuanced understanding of the development of the pathogenic Th17 cells, we may be able to pursue ways to regulate them or their function.”

Hafler said Kuchroo’s team worked on tracing how these immune cells were wired, and what triggered their development. They identified a specific gene known as SGK1 that plays an important role in the cells’ development. This gene had not been seen in T cells before, but it has been known to play a role in absorbing salt in the gut and kidneys.

“We put the two together and went after this,” Hafler said.

Researchers at Harvard and Yale and colleagues in Germany led by Dominik Mueller looked to see whether a high-salt diet could induce the destructive immune system response that is the hallmark of autoimmunity.

They found that adding salt to the diet of mice induced the production of Th17 cells and that mice genetically engineered to develop a form of MS had more severe disease than mice fed a normal mouse diet.

Hafler says the findings now need to be studied in people. He has already gotten permission to test the effects of lowering the salt intake in the diets of individuals with multiple sclerosis to see if their symptoms improve.

It likely be years before this link is confirmed, but Hafler says for patients already at risk of autoimmune disease, reducing dietary salt may be a good idea.

“If I had MS, I would think very much about not eating processed foods and really cutting down my salt intake,” he said.

SOURCE: www.foxnews.com

———————————————————————————————-

Salt link to multiple sclerosis unproven

Thu, 07 Mar 2013 13:33:00 EST

News that high-salt diets have been linked to autoimmune conditions has hit the headlines today, with BBC News reporting that “The amount of salt in our diet could be…leading to diseases such as multiple sclerosis.”

However, the BBC’s story is not based on trials of how much salt people eat and whether they go on to develop multiple sclerosis (MS), as you might expect. The story is actually based on studies looking at the impact salt has on immune cells, and how it affects the development of a condition similar to MS in mice.

MS is an autoimmune disease. These are diseases that occur when the immune system malfunctions, creating antibodies that attack the body’s own cells. In MS, the immune system attacks the cells that make up nerve fibres.

This study found that mice fed a high-salt diet produced more immune cells called T-helper 17 (TH17) cells, which are involved in some autoimmune diseases.

These results are food for thought about the role high-salt diets play in the development of autoimmune diseases. But because the study was carried out in animals, it is unclear if similar results would be found in people.

We can’t conclude that a high-salt diet causes MS from the results of this study. However, we do know that a high-salt diet is unhealthy and too much salt can cause high blood pressure.

Where did the story come from?

The study was carried out by researchers from Harvard Medical School, the Massachusetts Institute of Technology and the University of Salzburg, and was funded by the US National Institutes of Health and other research foundations in the US and Austria.

It was published in the peer-reviewed journal Nature.

The BBC report on the research was measured and accurate, emphasising that the findings were from early laboratory studies.

What kind of research was this?

This was a series of laboratory and animal studies investigating possible environmental triggers for autoimmune activity.

Experts suggest that genetics and gender play a key role in autoimmune diseases, but that environmental triggers are also a factor in the development of these disorders. The current research looked at the impact of salt on the production (or overproduction) of a specific type of immune cell, T-helper 17 (TH17) cells, which promote inflammation as part of an immune response.

One experiment moved beyond cells in a laboratory and looked at the effect of a high-salt diet on the development of a condition similar to MS, called experimental autoimmune encephalomyelitis (EAE), in mice.

As laboratory and animal studies, this series of experiments can provide clues about how salt may impact immune cell responses. However, they cannot tell us whether it directly affects the development of autoimmune diseases in people.

What did the research involve?

Several teams of researchers first looked into the molecular mechanisms that produce TH17 cells. This series of experiments suggested that a gene responsible for regulating salt levels in cells is involved in the TH17 cells signalling network (the series of molecular activity that enables communication between cells).

They found that when cells were exposed to increased concentrations of salt, this gene (SGK1) was activated and increased the development of TH17 cells. This finding led to the researchers conducting experiments using mice with EAE.

The researchers took three groups of mice:

  • group 1 lacked the SGK1 gene and was fed a normal diet
  • group 2 lacked the SGK1 gene and was fed a high-salt diet for three weeks
  • group 3 had the SGK1 gene and was fed the same high-salt diet as group 2

The researchers then determined whether the mice developed EAE so they could look at the role played in the disease by the SGK1 gene and salt exposure.

What were the basic results?

The researchers found differences between the groups in the number of TH17 cells produced, as well as the likelihood of the mice developing EAE, and the severity of the condition:

  • group 1 (which lacked the SGK1 gene and was fed a normal diet) had fewer TH17 cells and less severe EAE
  • group 2 (which lacked the SGK1 gene and was fed a high-salt diet) appeared to be protected against the development of EAE
  • group 3 (which had the SGK1 gene and was fed a high-salt diet) had more frequent and severe EAE than mice fed a normal diet, and more TH17 cells than group 2

How did the researchers interpret the results?

The researchers say that this data suggests that high salt intake allows for an increase in TH17 cells in a way that relies on the SGK1 gene activating. They feel this “therefore has the potential to increase the risk of promoting autoimmunity.”

Conclusion

This early stage research suggests that increased salt consumption may play a role in the production of a certain type of immune cell (TH17). The study further suggests that a high-salt diet can increase the rate and severity of an MS-like condition in mice (EAE).

These experiments are an interesting insight into the possible interplay between the genetic and environmental factors involved in autoimmune diseases. However, at this stage what this means for human autoimmune disease is not clear.

This research should certainly not be interpreted as meaning that a high-salt diet causes multiple sclerosis in people (although it can cause high blood pressure).

While the term ‘autoimmune diseases’ may seem to imply a similar set of conditions, there are in fact a variety of different autoimmune conditions. The different factors involved in these conditions is unlikely to be the same across all conditions.

The researchers say that while their results indicate that the gene SGK1 plays a key role in autoimmune responses, “it is likely that other immune cells and pathways are also influenced by increased salt intake,” and that their results “do not exclude additional alternative mechanisms by which an increase in NaCl [salt] affects TH17 cells.”

This means that these experiments outlined a possible way that a single environmental trigger (salt) could interact with a single gene (SGK1), and how this could influence the production of a type of immune cell (TH17 cells) that has been implicated in autoimmune disorders.

Other complex processes are likely to be involved, because many other cells also produce proteins that are involved in autoimmune disorders.

As the researchers themselves say, their results raise “the important issue of whether increased salt in westernised diets and in processed foods contributes to an increased generation of pathogenic [disease causing] TH17 cells and for an unprecedented increase in autoimmune disorders.”

A great deal more research is needed to find out whether, and how, salt consumption impacts on both the development and severity of autoimmune diseases in people. Such research could involve cohort or case control studies to establish whether or not there is a link between dietary salt intake and multiple sclerosis, or other autoimmune diseases.

Randomised controlled trials would be needed to firmly establish the role that salt plays in autoimmune conditions. Commentators point out that “the risks of limiting dietary salt intake are not great, so it is likely that several such trials will be starting soon.”

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Salt linked to immune rebellion in study. BBC News, March 7 2013

Could junk food increase your risk of MS, asthma and eczema? Scientists link salt to autoimmune diseases for first time. Mail Online, March 6 2013

Links To Science

Wu C, Yosef N, Thalhamer T, et al. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature. Published online March 6 2013

SOURCE :   www.ncbi.nlm.nih.go

Immunologists find a molecule that puts the brakes on inflammation

Christopher Hunter and Aisling O’Hara Hall

(Medical Xpress) September 28, 2012—We couldn’t live without our immune systems, always tuned to detect and eradicate invading pathogens and particles. But sometimes the immune response goes overboard, triggering autoimmune diseases like lupus, asthma or inflammatory bowel disease.

A new study led by University of Pennsylvania researchers has now identified a crucial signaling molecule involved in counterbalancing the immune system attack.

“The immune response is like driving a car,” said Christopher Hunter, professor and chair in the Department of Pathobiology in Penn’s School of Veterinary Medicine. “You hit the accelerator and develop this response that’s required to protect you from a pathogen, but, unless you have a brake to guide the response, then you’ll just careen off the road and die because you can’t control the speed of the response.”

The research to characterize this immune system “brake” was led by Hunter and Aisling O’Hara Hall, a doctoral candidate in the Immunology Graduate Group. Additional Penn collaborators included scientists from the Penn Genome Frontiers Institute’s Department of Biology and the Perelman School of Medicine’s Department of Medicine.Researchers from Merck Research Laboratories, the National Institute of Allergy and Infectious Disease, Harvard Medical School and Janssen Research and Development also contributed to the work, which was published in the journal Immunity.

“Healthy people have these cells—you have them, I have them—that are called Tregs,” or regulatory T cells, Hunter said. “If you don’t have them you develop spontaneous inflammation and disease.”

Different forms of regulatory T cells operate as the brakes on various kinds of inflammation, but, until now, scientists hadn’t been certain of how these Tregs became specialized to do their particular jobs.

Hall, Hunter and colleagues decided to follow up on a molecule called IL-27. Scientists used to think IL-27 played a role in causing inflammation, but, in 2005, a team of Penn researchers, including Hunter, found the opposite; it was actually involved in suppressing inflammation. Thus, when mice that lack IL-27 are challenged with the parasite Toxoplasma gondii, they develop overwhelming inflammation. ”

We never worked out how it did that, but it was a paradigm change at the time,” Hunter said.

In the new study, the researchers delved deeper into IL-27’s role. They found that exposing regulatory T cells to IL-27 promoted their ability to suppress a particular type of inflammation. The Penn-led team also demonstrated that they could rescue infected IL-27-deficient mice by giving them a transfusion of regulatory T cells. This finding suggests that IL-27 is required to produce the Treg cells that normally keep inflammatory responses in check during infection.

“Very surprisingly, we were able to show that the Tregs could ameliorate the pathology in this system,” Hall said. “We don’t think this is the only mechanism by which IL-27 limits immune pathology, but it sheds light on one mechanism by which it could be functioning.”

Further experiments showed that Tregs express a different suite of genes in the presence of IL-27 as compared to another molecule that has been implicated in this process, interferon gamma, or IFN-γ. The researchers’ findings indicate that the two molecules have division of labor when it comes to suppressing inflammation: IL-27 seems to be important in helping control inflammation at the site of inflammation, whereas IFN-γ appears more significant in the peripheral tissues.

“At the site of inflammation, where you’re getting your pathology, that’s where IL- 27 is important,” Hall said.

With a new understanding of how IL-27 may cause a class of Tregs to become specialized inflammation fighters, researchers have a new target for ameliorating the unwanted inflammation associated with all kinds of autoimmune conditions.

“Now we have a molecular signature that may be relevant in inflammatory bowel disease, in multiple sclerosis, in colitis and Crohn’s disease, in rheumatoid arthritis, in lupus,” Hunter said.

Next on tap, the team plans to study IL-27 in the context of asthma , lupus and arthritis.

More information: dx.doi.org/10.1016… .2012.06.014 J
Journal reference: Immunity
Provided by University of Pennsylvania

SOURCE: medicalxpress.com

Study on inflammatory bowel disease in First Nations people adds to understanding of disease

Inflammatory bowel disease is relatively rare in Canadian First Nations people but common in white people, possibly due to different genetic variants, according to a new study in CMAJ (Canadian Medical Association Journal) that helps improve understanding of the mechanisms of the disease.

Inflammatory bowel disease (IBD), a painful chronic immune disease that includes Crohn disease and ulcerative colitis, has a genetic predisposition. Studies in Manitoba in the 1990s found significantly lower prevalence rates of Crohn disease (16/100 000 people) and ulcerative colitis (56/100 000) than non-First Nations people: 209/100 000 people and 176/100 000 people respectively. However, they have higher rates of other autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus and ankylosing spondylitis (the latter is often found with IBD in other populations).

There have yet to be studies on the genetics of IBD in First Nations people, and this study by Canadian researchers helps expand the understanding of the mechanism of IBD.

Researchers from the University of Toronto and Mount Sinai Hospital, Toronto, and the University of Manitoba, Winnipeg, looked at DNA from 340 healthy First Nations people and 285 white participants from Manitoba who did not have any chronic immune diseases or first-degree relatives with a chronic immune disease. They focused on 69 different genetic markers for immune regulation called nucleotide polymorphisms (SNPs) that are associated, or suspected to be linked, with IBD.

“We found substantial genetic variation between First Nations and white people at loci associated with inflammatory bowel disease,” write Drs. Charles Bernstein, Director of the Inflammatory Bowel Disease Clinical and Research Centre, University of Manitoba and Travis Murdoch, Inflammatory Bowel Disease Group, Mount Sinai Hospital, and coauthors.

They found that First Nations people compared with white people had lower numbers of genetic variants involved in recognition of bacteria, which may impact how they respond to bacteria. A current favoured hypothesis as to the cause of IBD is that the bowel is reacting against bacteria present within the bowel lumen.

“There is a paucity of research chronicling the genetics of First Nations people in Canada, particularly in relation to immune-mediated inflammatory diseases,” write the authors. “However, the unique susceptibility and protection patterns in this population for complex diseases…make studying the genetics of First Nations people potentially insightful.”

Understanding which gene mutations are absent in groups who do not get a certain disease can help underscore which gene mutations may be the most relevant in the groups who do get the disease.

data from: medicalxpress April 10, 2012

 

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Related Link:

Prevalence of genetic variants associated with inflammatory bowel disease in a healthy First Nations cohort

Travis B. Murdoch, Charles N. Bernstein, Hani El-Gabalawy, Joanne M. Stempak, Michael Sargent, Brenda Elias, Wei Xu, Saad Pathan, Mark S. Silverberg

Abstract

Background: Inflammatory bowel disease is the result of both genes and environment. Canadian First Nations people, despite living in a region with a high prevalence of inflammatory bowel disease, are relatively protected from this disease. We aimed to compare the carriage of genetic variants associated with inflammatory bowel disease in healthy First Nations and white people.

Methods: DNA was extracted from the venous blood of healthy First Nations (n = 340) and white (n = 285) participants from Manitoba. Genotyping was performed for 69 single nucleotide polymorphisms (SNPs) with known or suspected associations with inflammatory bowel disease. We compared the genotypes between groups by logistic regression, adjusting for multiple testing. We calculated a risk score for the NOD2 gene by adding the number of risk alleles at three important NOD2 SNPs (G908R, R702W and 3020insC).

Results: We found genetic variation between white and First Nations participants at 45 of 69 SNPs. Notably, carriage of the ATG16L1 T300A mutation was lower in First Nations participants (p = 4.1 W 10-30). Cumulative carriage of important NOD2 variants was significantly lower among First Nations participants (3.9% v. 15.2%; p < 0.0001 for risk score) than among white participants. Risk variants in IL23R (p = 0.014) and IL12B (p = 1.2 W 10-16), among others, were more prevalent among First Nations participants than among white participants.

Interpretation: The low prevalence of variants associated with bacterial processing and handling in First Nations people may explain their relative protection from inflammatory bowel disease. Increased carriage of a number of risk variants, for example in the interleukin-23/Th17 pathway, is especially intriguing given their importance in other inflammatory diseases of high incidence in First Nations populations.

http://www.cmaj.ca/content/early/2012/04/10/cmaj.110613

 

Ankylosing Spondylitis and Undifferentiated Spondyloarthropathy

 

Why bad immunity genes survive: Study implicates arms race between genes and germs

University of Utah biologists found new evidence why mice, people and other vertebrate animals carry thousands of varieties of genes to make immune-system proteins named MHCs – even though some of those genes make us susceptible to infections and to autoimmune diseases.

นักชีววิทยาของมหาวิทยาลัยยูทาห์ พบหลักฐานใหม่ที่ว่าทำไมหนูคนและสัตว์มีกระดูกสันหลังอื่น ๆ จึงมียีนหลายพันสายพันธุ์ที่สร้างโปรตีนระบบภูมิคุ้มกันของร่างกายที่ชื่อ MHCs – แม้ว่าบางส่วนของยีนเหล่านั้นทำให้เราไวต่อการติดเชื้อโรคและไวต่อการเกิดโรคภูมิคุ้มกันผิดปกติ

This electron microscope image shows yellow particles of a mouse leukemia virus named Friend virus emerging or “budding” out of an infected white blood cell known as a T-cell. By allowing the Friend virus to mutate and evolve in mice, University of Utah researchers produced new evidence that an arms race between microbes and immune-system MHC genes is responsible for maintaining an amazing diversity of those genes, even though some of them are responsible for autoimmune and infectious diseases that make us sick. Credit: Elizabeth Fischer and Kim Hasenkrug, NIH

Major histocompatibility complex” (MHC) proteins are found on the surface of most cells in vertebrate animals. They distinguish self from foreign, and trigger an immune response against foreign invaders. MHCs recognize invading germs, reject or accept transplanted organs and play a role in helping us smell compatible mates.

“This study explains why there are so many versions of the MHC genes, and why the ones that cause susceptibility to diseases are being maintained and not eliminated,” says biology Professor Wayne Potts. “They are involved in a never-ending arms race that causes them, at any point in time, to be good against some infections but bad against other infections and autoimmune diseases.”

By allowing a disease virus to evolve rapidly in mice, the study produced new experimental evidence for the arms race between genes and germs – known technically as “antagonistic coevolution.” The findings will be published online the week of Feb. 6, 2012, in the journal Proceedings of the National Academy of Sciences.

Potts, the senior author, ran the study with first author and former doctoral student Jason Kubinak, now a postdoctoral fellow in pathology. Other co-authors were biology doctoral student James Ruff, biology undergraduate C. Whitney Hyzer and Patricia Slev, a clinical assistant professor of pathology. The research was funded by the National Science Foundation and the National Institute of Allergy and Infectious Diseases.

 

Theories for the Diversity of Immune-System MHC Genes

Most genes in humans and other vertebrate have only one or two “alleles,” which are varieties or variants of a single gene. Although any given person carries no more than 12 varieties of the six human MHC genes, the human population has anywhere from hundreds to 2,300 varieties of each of the six human genes that produce MHC proteins.

“The mystery is why there are so many different versions of the same [MHC] genes in the human population,” Kubinak says, especially because many people carry MHCs that make them susceptible to many pathogens (including the AIDS virus, malaria and hepatitis B and C) and autoimmune diseases (including type I diabetes, rheumatoid arthritis, lupus, multiple sclerosis, irritable bowel disease and ankylosing spondylitis).

Scientists conducted experiments that allowed a disease virus to evolve rapidly in mice. Credit: Wayne Potts, University of Utah

 

Scientists have proposed three theories for why so many MHC gene variants exist in vertebrate animal populations (invertebrates don’t have MHCs), and say all three likely are involved in maintaining the tremendous diversity of MHCs:

— An organism with more MHC varieties has a better immune response than organisms with fewer varieties, so over time, organisms with more MHCs are more likely to survive. However, this theory cannot explain the full extent of MHC diversity.

— Previous research indicates people and other animals are attracted to the smell of potential mates with MHCs that are “foreign” rather than “self.” Parents with different MHC variants produce children with more MHCs and thus stronger immune systems.

— Antagonistic coevolution between an organism and its pathogens. Kubinak says: “We have an organism and the microbes that infect it. Microbes evolve to better exploit the organism, and the organism evolves better defenses to fight off the infection. One theory to explain this great diversity in MHC genes is that those competing interests over time favor retaining more diversity.”

 

The Arms Race between Germs and MHC Genes

“You naturally keep genes that fight disease,” Kubinak says. “They help you survive, so those MHC genes become more common in the population over time because the people who carry them live to have offspring.”

Pathogens – disease-causing viruses, bacteria or parasites – infect animals, which defend themselves with MHCs that recognize the invader and trigger an immune response to destroy the invading pathogen.

But over time, some pathogens mutate and evolve to become less recognizable by the MHCs and thus evade an immune response. As a result, the pathogens thrive. MHCs that lose the battle to germs become less common because they now predispose people who carry them to get sick and maybe die. It was thought such disease-susceptibility MHC genes eventually should vanish from the population, but they usually don’t.

Why? While some of those MHCs do go extinct, others can persist, for two reasons. First, some of the now-rare MHCs gain an advantage because they no longer are targeted by evolving microbes, so they regain an ability to detect and fight the same germ that earlier defeated them – after that germ mutates yet again. Second, some of the rare MHCs can mount an effective immune response against completely different microbes.

 

How the Study was Performed; Implications of the Findings

The researchers studied 60 mice that were genetically identical, except the mice were divided into three groups, each with a different variety of MHC genes known as b, d and k, respectively.

A mouse leukemia virus named the Friend virus was grown in tissue culture and used to infect two mice from each of the three MHC types. The fast-evolving retrovirus grew within the mice for 12 days, attacking, enlarging and replicating within the spleen and liver. Virus particles in the spleen were collected, and the severity of illness was measured by weighing the enlarged spleen.

 

Many people carry MHCs that make them susceptible to pathogens like the AIDS virus. Credit: NIH

Then, virus taken from each of the first three pairs of mice (b, d and k) was used to infect another three pair of mice with the same MHC types. The process was repeated until 10 pairs of mice in each MHC type were infected, allowing the virus time to mutate.

In this first experiment, the biologists showed they could get the Friend virus to adapt to and thus evade the MHC variants (b, d or k) in the mouse cells it attacked.

Next, the researchers showed that the virus adapted only to specific MHC proteins. For example, viruses that adapted to and sickened mice with the MHC type b protein still were attacked effectively in mice that had the type d and k MHCs.

In the third experiment, the researchers showed that pathogen fitness (measured by the number of virus particles in the spleen) correlated with pathogen virulence (as measured by spleen enlargement and thus weight). So the virus that evaded MHC type b made mice with that MHC sicker.

Together, the experiments demonstrate “the first step in the antagonistic coevolutionary dance” between a virus and MHC genes, Potts says.

Potts says the findings have some important implications:

— The use of antibiotics to boost productivity in dairy herds and other livestock is a major reason human diseases increasingly resist antibiotics. Selective breeding for more milk and beef has reduced genetic diversity in livestock, including their MHCs. So breeding more MHCs back into herds could enhance their resistance to disease and thus reduce the need for antibiotics.

— Because their populations are diminished, endangered species have less genetic diversity, making them an easier target for germs. Potts says it would be desirable to breed protective MHCs back into endangered species to bolster their disease defenses.

— Genetic variation of MHCs in people and other organisms is important for limiting the evolution and spread of emerging diseases. In effect, Potts and colleagues created emerging diseases by making a virus evolve in mice. “It’s a model to identify what things change in viruses to make them more virulent and thus an emerging disease.”

 

Data from: medicalxpress , February 6, 2012

เซลล์ในตัวลิขิตตนเองได้ ลงเอยลงได้หลายรูปแบบ

นักวิทยาภูมิคุ้มโรคค้นพบสิ่งซึ่งเป็นการพลิกความรู้ในเรื่องสิ่งซึ่งกำหนดชะตากรรมของเซลล์เสียใหม่ ว่า เซลล์สามารถจะลิขิตชีวิตตนเองบางอย่างได้

นักวิจัยของสถาบันวิทยาภูมิคุ้มโรค ได้ความรู้จาก การศึกษา เซลล์บี.อันเป็นภูมิคุ้มโรค ซึ่งสร้างภูมิคุ้มกันว่า เซลล์บี.สามารถลงเอยได้หลายอย่าง ส่วนใหญ่มักจะตาย แบ่งตัวกลายเป็นภูมิคุ้มกัน หรือไม่ก็สร้างภูมิคุ้มกัน รูปแบบต่างๆ

โดยทั่วไปเชื่อว่า ปัจจัยภายนอก เช่น ฮอร์โมน บางชนิด หรือโมเลกุล เป็นตัวลิขิตชีวิตเซลล์ แต่ในการ ศึกษานี้ ศาสตราจารย์ฟิล ฮอดจ์กิน หัวหน้าแผนก เผยว่า ส่วนใหญ่แล้วขบวนการภายในของมันเป็นตัวกำหนด “เซลล์ทำตัวเหมือนกับมีเครื่องจักรกลในตัวควบคุมอยู่ เครื่องจักรนั้นคงเหมือนกับนาฬิกา หรือเครื่องจับ เวลาของการแบ่ง การตายแบบชนิดของภูมิคุ้มกันที่ผลิต”.

ที่มา: ไทยรัฐ 16 มกราคม 2555

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Cells Influence Their Own Destiny

To understand in a big shake-up of scientists, which will determine the fate of cells, researchers at the Walter and Eliza Hall Institute, show that the cells only control their own destiny to be.

Researchers from the Institute of Immunology Division, drew their conclusion after studying the B-cells, immune cells to produce antibodies.

B-cells, several fate. Some of the most common to die of his fate, to divide, an antibody-secreting cell antibodies or what to change it. All this happens while the cells in the lymph nodes are proliferating.

The general view is that a-cell fate by external stimuli, as determined as the presence of certain hormones and cell signaling molecules.

However, the said Walter and Eliza Hall Institute of Immunology head, Professor Phil Hodgkin and his colleagues Dr. Mark Dowling, Dr. Cameron Wellard and Ms Zhou Jie, that the cell fate is largely determined by internal processes.

To check their theory development back to the research team, the conditions for the B-cells into different cell types, and then filmed the cells, working with Dr. John Markham of the National Information and Communication Technology Australia, new technologies and methods of image analysis to develop.

The research team from the experimental observations were strengthened by the experience of mathematical Dr. Ken Duffy from the Hamilton Institute at the National University of Ireland Maynooth. Dr. Duffy was critical understanding of the opportunities interpret were filmed for the team with the implementation of the 2500 cells. The team’s findings were recently published in the journal Science.

Professor Hodgkin said that the cells, as if the internal machinery that cells behave the fall fate. “Each of these machines is like an internal clock or timer for the division, death, what type of antibody they produce and whether they are antibody-secreting cells,” he said.

Dr. Dowling explains the different fates of results is a game. “Each cell in a sense, the establishment of a ticking clock for each of the results and all the bell goes off first is the decision that the cell starts,” he said. “The cell tries anything to win than to just do a lot.”

Professor Hodgkin said that although the cells were given the same external signals, there are considerable differences in what happened to the cell population. “A reliable part of the B-cells with each of the different fates would end,” he said. “This suggests that external factors such as hormones and cell signaling molecules, cells, not what they should do, to tell, but the probability of changing what the cells do anyway.”

When the body reacts to infection, many cell types, each producing a different function. Dr. Dowling said, it could be that the body has a chance to optimize the production of certain cell types, depending on the situation was. “The body produces many different hormones and cell signaling proteins, so the odds are for different infections. A lot of molecules involved in the immune system respond to this opportunity.”

Professor Hodgkin said the hope was now mathematical models of how the external signals, the probability that an immune cell population predict create change. “The development of such models would help in the development of new immunotherapies for the treatment of autoimmune diseases and better vaccines,” he said.

This study was supported by the National Health and Medical Research Council of Australia, the Victorian Government and the Science Foundation Ireland.

Data from: www.sowscience.com

In division or death, research finds cells in charge of their destiny

Date: January 11 2012
Jackie Hanafie and Damien Currie

MELBOURNE researchers have found that the body’s immune cells have a greater control over their own destiny than previously realised, prompting a shake-up of scientists’ understanding of how cells work.

The findings, by researchers from the Walter and Eliza Hall Institute in Parkville, will aid future drug design for a range of conditions including diabetes, some infectious diseases, rheumatoid arthritis and allergies such as hayfever.

After studying B cells – immune system cells that can make antibodies – the researchers discovered that cells were not necessarily instructed by their exposure to hormones and their external environment, as originally thought.

A B cell is a type of blood cell that belongs to a group of white blood cells called lymphocytes, which are crucial in protecting the body from infection.

B cells are an essential component of the adaptive immune system.

Head of immunology Professor Phil Hodgkin, who led the study, said it showed that this was not actually the case, with the cells being involved in an internal decision-making process.

”Each cell has the potential to divide, to die, to change the type of antibody it makes,” Professor Hodgkin said.

”This all happens while the cells are proliferating in the lymph nodes.”

Mark Dowling also worked on the study alongside colleagues Jie Zhou, Cameron Wellard and John Markham.

Dr Dowling explained the results as the different outcomes being in competition with each other.

”Each cell will, in some sense, set up a clock that starts ticking for each of the outcomes and whatever clock goes off first is the decision that the cell makes,” he said.

“The cell is trying to do everything but only one fate wins.”

The study, which was supported by the National Health and Medical Research Council of Australia, the Victorian government and Science Foundation Ireland, involved filming a recreation of the conditions necessary for B cells to develop into different cell types.

Professor Hodgkin said the hope is now to create new models that will help in the design of new immune therapies for autoimmune diseases and improved vaccines.

The study took place over a four year period and was recently published in the international journal Science.

This material is subject to copyright and any unauthorised use, copying or mirroring is prohibited.

Data from: www.theage.com.au