Health Meaning

Designer antibodies can rid the body of the AIDS virus -

Anti-HIV drugs have prolonged millions of lives, but they have not eliminated the virus from person. Indeed, HIV integrates its genetic material in the chromosomes of certain white blood cells, helping him to escape the attention of the immune system. Two new studies show that artificial antibodies could "redirect" the immune response to these latently infected cells and help drain the HIV reservoirs in the body. But this creative strategy also carries risks.

"The reason is sound, and data are exciting, but we need to move cautiously," said Steven Deeks, a clinical HIV / AIDS at the University of California, San Francisco (UCSF) , which tests the healing strategies. "There's really no room for error."

Several previous studies have investigated whether drugs can shock the cells that are infected with latent HIV to make new virus, setting them up for the kill by the natural immune response. But this new work ups the ante by developing so-called bispecific antibodies that both promise to reverse the lag and do the job of raking. "the dual activity makes this interesting new approach," said Sharon Lewin, a researcher cure HIV who heads the Peter Doherty Institute for Infection and Immunity in Melbourne, Australia. "It's exciting."

The two new documents that appear only online to date, mainly involving experiments test tubes. One, described in Nature Communications today ' hui, was conducted by a team from the vaccine research Center at the US National Institute of allergy and infectious diseases (NIAID) in Bethesda, Maryland. the second study was published last month in the Journal of Clinical Investigation ( JCI ) and involved a collaboration between three universities and a biotechnology company.

both groups artificial versions designed antibodies, the molecules form Y performed by the immune system to target pathogens. In natural antibodies, the two "arms" of the Y enclose the same target. However, the antibody arm bispecific each capture a unique protein. In this case, the two teams their antibodies designed to hug an HIV protein and CD3, a receptor present on the surface of white blood cells.

The bispecific antibodies focus on CD3 receptor for two reasons. The first is that the HIV hides within the DNA of white blood cells or T lymphocytes, which have CD3 receptors. The other is that a second type of CD3-studded lymphocytes cells known as killer T name destroys cells infected with HIV.

The bispecific antibody binds to CD3 first on cells harboring latent HIV. This prompts the cells to divide, a process of "activation" that awakens the virus of sleep. new proteins by HIV are then produced that migrate to the cell surface.

However, the bispecific antibody captures a killer T cell that has a CD3 receptor and with its second arm, is a newly activated cell that HIV proteins on its surface. Bring the killer T cell near the infected cell effectively shoves prey in the lion's mouth. "The molecule works the way you want to hope that it would be in several trials," said John Mascola, director of the NIAID Vaccine Research Center and leader of the group reporting of Nature Communications study.

But no team has yet shown that their bispecific antibodies can effectively reduce HIV reservoirs in monkeys, which are commonly used to study the AIDS virus. These studies are ongoing, and it will take at least a year before either team tests concepts in people infected with HIV. David Margolis, a virologist at the University of North Carolina, Chapel Hill, and co-author of the study JCI , said drain a reservoir ultimately may require combination with bispecific antibodies other reversing latency approaches and immune system stimulators such as HIV vaccines.

Deeks of

UCSF warns that anti-CD3 antibodies can cause too much activation of T cells, leading to a massive inflammatory reaction that damages organs and can even cause death. Indeed, in a 1999 study of anti-CD3 antibodies used for purging the tanks of three people infected with HIV, severe side effects, including kidney failure and seizures surface quickly. But the anti-CD3 antibody in the previous study were the two arms, Mascola ratings, which leads to the activation much more than the single arm in the new bispecific antibodies. It also emphasizes that two bispecific antibodies cancer on both the market have anti-CD3 arms. "The key is to find the right balance between activation and toxicity CD3" said Mascola. "That's the real challenge here."

Vitamin C kills the tumor cells with difficult to treat mutation -

Maybe Linus Pauling was on to something after all. There decades chemist Nobel Prize has been relegated to the periphery of medicine after defending the idea that vitamin C could fight against a host of diseases, including cancer. Now a study published online today in Science reports that vitamin C can kill tumor cells that carry a mutation common cancer-causing and - mice can slow growth of tumors with the mutation.

If the results hold in people, the researchers could find a way to treat a wide band tumors that lacked effective drugs. "This [could] be an answer to everyone fighting for," says molecular biologist Channing Der, University of North Carolina, Chapel Hill, one of many researchers who are trying to target cancers with mutation. The study is also rewarding for the handful of researchers who pursue vitamin C or ascorbic acid as a drug against cancer. "I'm encouraged. Maybe people will finally pay attention, "says vitamin C researcher Mark Levine of the National Institute of Diabetes and Digestive and Kidney Diseases.

In 1971, Pauling began collaborating with a Scottish doctor who had successful treatment of cancer patients with vitamin C. But the failure of two clinical trials of vitamin C pills, carried the late 1970s and early 1980s at the Mayo Clinic in Rochester, Minnesota reported, dampened enthusiasm for the idea of ​​Pauling. Studies conducted by Levine's group later suggested that vitamin must be administered intravenously to reach high enough doses to kill cancer cells. Some recent small trials over the five years - to pancreatic and ovarian cancer - suggested that the treatment of IV vitamin C combined with chemotherapy can prolong survival Cancer. But skeptics are not influenced. "The atmosphere was poisoned" by previous failures, says Levine.

there

A few years Jihye Yun, a graduate student at Johns Hopkins University in Baltimore, Maryland, found that colon cancer cells whose growth is driven by mutations in the gene KRAS or less frequently mutated gene, BRAF , make exceptionally large quantities of a protein which transports glucose across the cell membrane. The carrier, GLUT1, provides the cells with high levels of glucose they need to survive. GLUT1 also carries the oxidized form of vitamin C, dehydroascorbic acid (DHA) in the cell, bad news for cancer cells, because Yun found that DHA may deplete the supply of a cell of a product chemical that sops free radicals. Because free radicals can harm a variety of ways cell, the conclusion suggested "vulnerability" if the cells were flooded with DHA, says Lewis Cantley at Weill Cornell Medicine in New York City, where Yun is now a postdoc.

[1945018laboratoireetcollaborateurs] Cantley found that high doses of vitamin C actually kill colon cancer cells cultured with BRAF or KRAS mutations by increasing levels of free radicals, which in turn inactivates an enzyme needed to metabolize glucose, depriving the energy cells. Then they gave daily injections of high doses - equivalent to a person eating 300 orange - to modified mice to develop KRAS focused on tumors colon. Mice developed fewer and smaller tumors colon compared to control mice.

Cantley hopes to soon start clinical trials that select patients with cancer based on KRAS or BRAF mutations and possibly GLUT1 state. New research from his group "indicates you should get the drug and who should not," he said. Bert Vogelstein cancer geneticist at the University Johns Hopkins, in whose laboratory Yun GLUT1 noticed the connection, is excited about the therapy of vitamin C, not only as a possible treatment for KRAS -mutated colon tumors, which account for about 40% of all colon cancers, but also for pancreatic cancer, a usually fatal cancer caused by KRAS . "No KRAS -targeted therapeutic emerged despite decades of effort and hundreds of millions of dollars [spent] industry and academia," says Vogelstein.

D others warn that the effects observed in mice may not hold up in humans. But because the high dose vitamin C is already known to be safe, says the researcher Vuk Stambolic cancer of the University of Toronto, Canada, oncologists "can quickly move forward in the clinic."

a disadvantage is that patients have to come to a clinic for infusions of vitamin C, ideally every day for months because vitamin C seems to take this time to kill cancer cells, Levine notes But Cantley said, it may be possible to make an oral formulation that reaches high levels in the blood -.. can be a way to get companies interested in sponsoring testing

How agriculture has changed the European - genome

When the first farmers plowed the Middle East in Europe 8500 years ago, they brought with them more than one style life, they also set in motion changes in genes that have changed the way Europeans looked digested food, and adapted to the disease. In a new study published in Nature today, an international team to sequence ancient DNA from 230 people who lived there 3000 years 8500 in Europe, Siberia, and Turkey. Their sample included the first ever sequenced DNA of the first farmers in the Middle East, as it buried in Barcin Höyük northwest of Anatolia, in Turkey today. The team reported earlier this year how natural selection has favored the spread of genes of white skin, tallness and digest the sugars in milk. In today's paper, the same researchers sequenced the DNA of more skeletons and found that the transition to agriculture also promoted the genes for digesting fat and immune genes that protect against disease infectious diseases, such as tuberculosis and leprosy. Interestingly, the team also found the spread of two variants of genes associated with celiac disease. These variants may have been favored because they help to compensate for a deficiency associated with certain regimes-in an amino acid called agricultural ergothioneine. But variants also have the secondary effect of stimulating Crohn's disease and other celiac disease.

Campaign against tuberculosis is intensifying its ambitions -

Your poor diet could hurt the bowels of your grandchildren -

Here's another reason to eat your vegetables. Trillions of microbes in the large intestine known as the human microbiome-dependent fiber prosper and give us energy. As the consumption of fibers decreases, so, too, is the range of bacteria which can survive in the intestine. Now a new study of several generations of mice fed a diet low in fiber indicates that this diversity dives deeper with each generation, a hint of what might occur in the human intestine as we continue to eat a diet of contemporary refined foods. The work may also help explain the rise in many Western diseases, such as inflammatory bowel disease and obesity.

"This is a seminal study," said Jens microbial ecologist Walter of the University of Alberta in Canada. "The extent by which the weak [fiber] supply depletes the microbiome in mouse experiments is striking."

For much of human history hunter-gatherer and early agricultural times, the daily fiber intake was probably at least three or four times the officially recommended today (something like 100 grams against 25 grams) -and several times higher than the average consumption in the United States today (15 g). the tendency has led many researchers, including Erica Sonnenburg microbiologist from Stanford University in Palo Alto, California, to suspect that the low well documented diversity of gut microbes in people in developed countries, 30 % less diverse than modern hunter-gatherers- is in part a product of considerably reducing the consumption of fibers.

the new study confirms this relationship in rodents. Sonnenburg and his colleagues raised mice in a germ-free environment, then fed them human faeces, giving them the human intestinal bacteria. When fed a diet low in fiber (about 30% less fiber than the chow control high fiber), animals experienced a significant dip in the gut microbial diversity (with about 60% of microbes lose at least half their populations). The mice then maintained on the food poor in fiber and have helped raise the offspring produced with a diversity even lower, the team announced today online Nature . And subsequent generations of mice fed low fiber continued to lose whole groups of microbes such as bacteria have reached these reduced numbers in the parents that they could not be transmitted through birth, nursing, or even tend to eat'S mouse droppings on the other.

by the fourth generation, mouse microbiota seemed to have reached a new normal, low steady microbiota diversity, accommodation only over a quarter of the diversity enjoyed by the first generation. In particular, no low generations fiber could be "saved" by reintroducing foods rich in fiber. To reach the bacterial variety of their grandparents, mice need a fecal transplant group rich in fiber and a diet rich in fiber.

The results raise questions about how our diet affects our own offspring. "As we move relatively little change in our human DNA for each generation, this study indicates that we potentially pass on huge changes in our gut microbiome," Sonnenburg said. Because the mice in this study started with microbes of a Westerner, the microbiome was already low in diversity, the study also suggests that "it may be possible for Western microbiota to lose the extra diversity," she adds. Microbiologist Eric Martens, University of Michigan Medical School in Ann Arbor, amazed by the extent of the loss. "The surprise is that the proportion of organizations can actually be driven to extinction," he said.

The researchers have yet to prove that the same rapid reduction of microbial diversity occurs on rights generations and if it is, what it means for health. "in these complex ecosystems, it is very difficult to know the exact result of the loss of biodiversity," said Sonnenburg. But, she notes, "it is likely that these extinctions in the microbiota have big effects." For example, other research has shown that obese people are more likely to have the lowest microbial diversity in their guts that their lean peers. and our more macroenvironments studies teach us that a diverse ecosystem is heartier and quicker to bounce to another less diversified.

Meanwhile, as Martens suggests in an accompanying commentary in Nature , "you might consider choosing a salad ... or an additional portion of beans."

Zika virus: Answers to Your Questions -

Where the Zika virus come from

First isolated in 1947 and first described in an article? 1952 Zika has long been known to occur in Africa and South Asia, but until there ten years, less than 15 cases have been described in the scientific literature. In 07, the virus caused a large outbreak in Yap, a group of islands in the western Pacific that is part of the Federated States of Micronesia; since then it has made a major tour of other Pacific islands before he landed in Brazil, where he began to spread quickly to other parts of South America, Central America, Mexico and the Caribbean.

Why has it exploded so suddenly

there may have been large epidemics in Africa and Asia in the past that was not detected ?; scientists did not pay much attention. But the current epidemic is a massive event waiting to happen. Latin America has a large number of A. aegypti , also known as the yellow fever mosquito, an important vector for Zika. (The tiger mosquito, A. albopictus , which is on the rise around the world, is considered a vector as well.) In addition, in the Americas had immunity to the virus. Travel makes things worse. Aedes mosquitoes do not fly more than a few hundred meters during their life; Zika moves from city to city and country to another when infected people receive on cars, buses, trains and planes.

These factors combined mean that the virus has the ability to spread far and fast once he had arrived.

Will Zika across the United States and Europe?

the United States and Europe have already seen "imported cases" -the people who arrived a Zika affected countries carrier of the virus. This was widely expected given the size of the epidemic in Latin America. The key question is whether there will be local homes-that is, the mosquitoes spread the virus from person to person. There is certainly a chance; A. albopictus occurs in several countries in Southern Europe (and it can move to the north), while the southern and eastern United States have populations of both A . aegypti and A. albopictus .

If so, scientists expect epidemics to be much lower than anywhere else on the basis of past experience with diseases transmitted by mosquitoes. Recent outbreaks of dengue fever in Florida, Texas and Hawaii were not sickened more than a few hundred people, for example; an outbreak of a disease transmitted by mosquitoes called chikungunya in northern Italy in 07, which began when a man infected with the virus arrived from India-ended after 197 cases. One reason that the epidemics in these countries tend to be smaller may be that people spend less time outdoors and live in homes that are harder for mosquitoes to enter; the size of mosquito populations may play a role as well.

Do we know for certain that Zika is causing an increase in birth defects?

No. There are strong indications that the areas in Brazil hit hard by Zika experienced a sharp increase in the number of babies born with microcephaly, a condition in which the head is much smaller than normal because the brain fails to develop properly. But it will take at least several months before results of the first case-control studies of pregnant women infected with Zika are available. Doctors in Brazil first noticed the increased cases of microcephaly for ultrasounds for pregnant women in June and July, months after the surge of Zika infections. expert in fetal medicine Manoel Sarno, who works at the Federal University of Bahia, said the pattern of brain damage he sees now appears separate from microcephaly caused by other infections, such as cytomegalovirus (CMV) or rubella. He and his colleagues began a study in August following Zika infected women during pregnancy; the results could come out late summer. Similar studies are underway elsewhere in Brazil and Colombia.

Are there other pressing issues that the scientists involved?

Plenty. Scientists are struggling to determine who was infected and who is not because the diagnostic tests have limitations. The tests, which detect the most accurate of the viral RNA in the blood of patient work within a week of the first symptoms appear. After this period, researchers can test the antibodies in the blood. But current testing for Zika antibodies cross-react with antibodies to dengue, which is so widespread in Brazil and much of the rest of Latin America-that almost all adults have antibodies to it. It is therefore difficult to say whether the mother of a baby born with microcephaly has been infected by Zika earlier in her pregnancy.

The researchers would also like to know how often Zika is transmitted through sexual contact. American scientist who caught the virus in Africa adopted his wife after getting home in 08, and a second case of alleged sexual transmission arrived in French Polynesia in 2013. But researchers have no idea what that risk is . ( "If I'm a man and I'm symptoms Zika, I wait a few months before having unprotected sex," virologist Scott Weaver of the University of Texas Medical Branch in Galveston recently said The New York Times .)

What drugs are available against Zika?

None. Until last year, Zika was so rare, and believed to be so sweet, that nobody cared to look for drug candidates. Even now that the virus is surging, it is not obvious that there is a large market for an antiviral drug, because the vast majority of infected people have very . few symptoms or none at all and it is not known that a drug could prevent birth defects when women Zika contract during pregnancy when they become infected and develop symptoms, it may be too late to avoid such damages. A vaccine against Zika can offer more hope to prevent microcephaly.

And when can we expect a vaccine?

It will take years. Several groups have started making vaccine candidates Zika, a process that will take at least several months. Most of these vaccine approaches are piggybacking on existing vaccines. For example, many vaccines are made by assembling proteins from the surface of a pathogen in a harmless virus or vector; who is now with Zika tried using these vectors. Once a candidate is made, it should be tested in animals before humans.Human tests start with small safety studies and move on to larger studies that verify if the product candidate is working. All it usually takes 10 to 15 months. Given the urgency, the time may be compressed, but even so, Anthony Fauci, director of the US National Institute of Allergy and Infectious Diseases, said STAT he can be at least 5 to 7 years before that a Zika vaccine is commercially available.

So what can we do to stop the spread of the virus?

stop mosquitoes from biting people. Countries and communities can try to reduce mosquito populations by eliminating small reservoirs such as water flower pots, empty bottles, and scrap tires that Aedes mosquitoes like to breed. People can also reduce their especially significant personal exposure for women who are or may become pregnant by putting screens on windows, covering their skin, and using insect repellent. However, history has shown that the impact of the fight against mosquitoes on epidemics is modest at best, and they are difficult to maintain.

There must be better ways to fight against mosquitoes?

Not yet, but they are in the works. A British biotech called Oxitec, which was recently bought by Intrexon, a US company, has developed synthetic biology A. aegypti mosquitoes containing a gene construct that will kill their offspring before they reach the age adult. When a substantial number of males of this strain are released into the wild, they will mate with local females produce offspring that are not viable, which has been shown to make a dent in the population.

In another line of research, scientists infect A. aegypti with a bacterium called Wolbachia , which reduces the ability of mosquitoes to transmit diseases. developing the researchers, these approaches were mostly thinking about dengue, but the rise of Zika is to give their efforts a new sense of urgency. But again, it will take several years before these strategies are ready for prime time.

Microbes in the gut right help children grow -

Why high "good" cholesterol may be bad news -

The 67-year-old woman had sky-high high-density lipoprotein (HDL) cholesterol to form long considered as protective against heart disease, yet his arteries were lined plate. His paradoxical cases helped motivate a team of scientists to show how high HDL can sometimes be a signal not of heart health, but the opposite :. A system incapable of siphoning fatty particles from circulation cholesterol

In the past 10 years, HDL particles have confounded scientists. The normal role of these beams of protein and lipid is to transport cholesterol in the liver rest of the body, which eliminates from the body. More something good should mean better health, and people naturally have higher HDL levels are usually better. But drugs that increase HDL cholesterol have flopped in clinical trials, and the genes that help raise does not seem to follow with less heart disease. "Nothing ever single HDL" said Jay Heinecke, a biochemist at the University of Washington, Seattle, who has studied for years.

In this week's issue of Science Daniel Rader, a geneticist and lipidologist at the University of Pennsylvania, and colleagues suggest that the amount of HDL is less important than the way it is effectively moved the arteries in the liver. the inspiration of Rader was a model mouse developed by Monty Krieger at the Massachusetts Institute of Technology in Cambridge there about 20 years. the mouse developers had deleted a gene called SCARB1 , resulting in animals with surprisingly high HDL and, just amazingly arteries severely blocked. "the mice actually receive heart attacks," said Heinecke. Indeed, the cholesterol displacement system outside the body is broken in these mice.

particles Normally HDL cholesterol gather immune cells that line the arteries, then deposit their load in the liver so that the cycle can begin again. The protein made by the SCARB1 gene, known as SR-B1, helps make this deposit occurs. Mice without SR-B1 have HDL particles swollen with cholesterol, struggling to attract more away from the arterial wall.

Rader wondered if the same could occur in some people. He and his colleagues began by sequencing the gene in 852 people with high HDL and 1,000 controls. They found a person of 67 years, women who had no copies of operation of SCARB1 gene and had more plaque on the arteries mean that a woman of her age. His HDL was 152 mg / dL, well above the average of about 62 mg / dl in women in her age group. Eighteen others were just a functional copy SCARB1 instead of the usual two, and most of them also had higher HDL. Detailed studies of nine people with SCARB1 mutations, including women, have suggested that in mice, their abundant HDL failed to effectively carry cholesterol throughout the body.

Rader then spread to his colleagues who had collected the DNA of hundreds of thousands of people for studies of lipids and heart disease. Among them, he found another 284 people who have had a single copy operation SCARB1 . (No one else was like the first woman with two missing copies.) Most of these people were also higher than average HDL. They were also 80% more likely than the witnesses CHD-roughly the same increase in risk seen traditional risk factors such as diabetes and hypertension.

"This is a key indication of what people have suspected from animal studies," says Alan Tall, an HDL researcher at Columbia University. It seems that HDL is higher "because the flow is blocked, "not because HDL excels in maintaining cholesterol on arteries.

Yet because Rader could find so few people without fully operational SCARB- 1 and because the potential effects of mutations on heart health appeared modest, the link between transport defective HDL and heart disease is still fragile, he and others say. and HDL behavior in a box Petri does not necessarily reflect what it does to the body, suggests Kuivenhoven Jan Albert, who studies the genetics of lipid metabolism at the University Medical Center Groningen in the Netherlands. "We have no good ways do the tests with HDL that can really say what happens "in a person, said Kuivenhoven.

HDL remains extraordinarily complex, and Rader Kuivenhoven say. It is possible that the collection of HDL drugs failed in clinical trials because of the type of HDL-products detected drugs doctors larger HDL particles than expected. Overall, however, there is little doubt that high HDL always follows with a healthier heart for most people, except, Rader said, when it does not.

Ultimately, he said, we would be able to say, "Your HDL is high because X which is good," and someone else, "Your HDL is high because of Y, which is a bad thing. "now, he and others want to nail down exactly what these factors might be and, potentially, how to run them off.

Local immunity goes -

Parasitic worms may prevent Crohn's disease by modifying the bacterial balance -

Parasitic worms that hide in the intestines of some people may be revolting, but they seem to prevent disease Crohn and other types of inflammatory bowel disease (IBD). A new study may explain how revealing that to allow beneficial microbes in the gut to supplant the bacteria that promote inflammation. The findings could lead to new ways to treat diseases of the gut by mimicking the effects of parasites.

"It is a beautifully made paper," says immunologist Joel Weinstock of Tufts University in Boston, who was not connected to the work. "It has not been shown previously that one of the mechanisms [of IBD] is through changes in the intestinal flora."

In people with IBD, inflammation in the results of digestive symptoms such as diarrhea and bleeding and can sometimes lead to bowel obstructions or other serious complications. Because parasitic worms, or helminths, can be harmful, they seem to be unlikely allies against these diseases. "They are called parasites for a reason," says immunologist Ken Cadwell of the New York University School of Medicine in New York City, co-author of the new study. However, the EIA is rare in parts of the world where helminths are prevalent, and it is surging in most developed countries, where few people now carry intestinal intruders. This difference suggests, the researchers say they are protective.

to determine how to could be our frenemies, Cadwell and his colleagues tested mice with the same genetic defect found in many people with Crohn's disease. mucus secreting cells in the bowel dysfunction in animals, reducing the amount of mucus that protects the intestinal mucosa of harmful bacteria. the researchers also detected a change in the microbiome rodents, the natural microbial community in their guts. The abundance of a microbe, an inflammation-inducing bacteria in the Bacteroides rises in mice with the genetic defect.

The researchers found that feeding rodents a type of intestinal worms restored their mucus-producing cells to normal. At the same time, the levels of both indicators of inflammation decreased in the intestines of animals. In addition, the range of bacteria in the intestines of displaced rodents, the team announced today online Science . Bacteroides numbers have plunged, while the prevalence of species in a different microbial group, Clostridiales increased. A second species of worm also trigger similar changes in the intestines of mice, the team confirmed

To check whether helminths cause the same effects in people, the scientists compared two populations in Malaysia :. Urban population living in Kuala Lumpur, which harbor some intestinal parasites, and members of indigenous groups, the Orang Asli who live in a rural area where worms are common. One type of Bacteroides proinflammatory microbes, predominated in the people of Kuala Lumpur. It was rarer among Orang Asli, where a member of Clostridiales group was plentiful. Orang Asli treat with drugs to kill their intestinal worms reversed this trend, favoring Bacteroides species on Clostridiales species, the team documented.

Cadwell and his colleagues also asked whether Clostridiales and Bacteroides microbes disagreed with others. They analyzed two sets of data on the frequencies of different gut microbes, which include results for American healthy residents and children in North America who have IBD. They saw the same relationship when Clostridiales species are in place Bacteroides varieties are down, and vice versa.

The findings of the study suggest that parasitic worms deliver their benefits indirectly through their impact on the microbial mix in the intestines. Worms are "having an anti-inflammatory effect by kicking something that is inflammatory," said Cadwell. Clostridiales group members can get a boost when worms are around, he said, because the intestines produce more mucus, bacteria feed on.

"This is a good proof of concept," says Gabriel Nunez immunologist at the University of Michigan, Ann Arbor, who was not connected to the research. It supports "the principle that some of these diseases may be related to changes in the microbiome. "But he warned that researchers still need direct evidence that Bacteroides species are responsible for Crohn's disease.

turn the results into a treatment for IBD could be difficult. Two recent clinical trials helminth treatment for Crohn's disease, in which participants drank a solution containing worm eggs, stopped early because the results been disappointing. These studies may not be the last word, however. Cadwell said the worm therapy might work in more or less 30% of Crohn's patients who have the same genetic defect as mice. and Weinstock noted that if researchers can determine how parasites trigger the change in the composition of microbe, "we may be able to bypass and develop a small molecule drug to achieve the effect of a safe manner."