Restore the natural barriers to intestinal infections through diet and pharmacological intervention can be a therapeutic option in cases of intestinal diseases like Crohn’s disease. This is according to a study published today in Proceedings of the National Academy of Sciences, conducted by a team from the Pasteur Institute of Lille, France. Mathias Chamaillard is the lead author.

The work’s protagonist is the role of the protein PPAR-gamma, regulator of antimicrobial peptides in the gut. The authors sought to determine whether this protein could act as protective against Crohn’s disease and other inflammatory conditions, and found in mouse model genetically engineered to be deficient in PPAR-gamma, there was a clearly reduced ability to fight infection bacteria in the colon compared with control models.

Reduced expression

In addition, researchers have found that colon biopsies of human specimens diagnosed with Crohn’s disease also have significantly reduced expression of antimicrobial peptides regulated by this protein.

Faced with these data, Chamaillard and his team suggest that both nutritional regimes such as certain drugs might improve the rehabilitation of dependent antimicrobial barriers PPAR-gamma in the gastrointestinal tract. This approach would help in the prevention of chronic injuries related to the onset of the disease.

The work is based on the leading role that has PPAR-gamma in intestinal homeostasis. It has been shown to act as an antimicrobial factor by maintaining the epithelial expression of beta-defensins colonies in the colon (from mDefB10 DEFB1 in mice and humans.)

Researchers have observed that the colonic mucosa of animals mutant for PPAR-gamma eliminates some of the main components of the intestinal microbiota, such as Candida albicans, Bacteroides fragilis, Enterococcus faecalis and Escherichia coli. As described, the neutralization of colonic activity, using an antibody anti-mDefB10 blocker, is effective in systems dependent on PPAR-gamma.

Also reveal the presence of a functional promoter variant required for the expression of DEFB1, which gives special protection against Crohn’s disease. This information has allowed the authors point out that the relationship with the disease of the colon is specifically linked to reduced expression DEFB1, irrespective of inflammation.

A serious bacterial or viral infection in the digestive system, called infectious gastroenteritis, could lead to irritable bowel syndrome, perhaps by generating a low-grade intestinal inflammation, according to Dr. Alex Ford Medical Center at McMaster University in Hamilton, Ontario.

Previous studies had suggested that such infections may be also associated with functional dyspepsia, which includes symptoms of acid reflux, satiety and indigestion of unknown cause, but without solid evidence.

The team studied a group of people in the small rural town of Walkerton, Ontario, during an outbreak of bacterial gastroenteritis occurred in 2000 by contamination of municipal water supply with cattle feces.

At that time became ill at least 2,300 people and seven died.

After two years of the epidemic, the team collected a representative sample of the population of that locality. In 2008, the team conducted a follow-up among 1088 control participants, two thirds of whom had become ill in the outbreak.

40 percent of the group had symptoms of dyspepsia, acid reflux, and uncomfortable sensations of fullness after eating, they said.

Half of those who had become ill during the outbreak of gastroenteritis had dyspepsia, unlike 30 percent of those who were not sick. The risk was twice as high for victims of the epidemic and that continued after further restrict the definition of indigestion.

For the team, the results suggest that intestinal infections “can trigger symptoms in the upper and lower gastrointestinal tract with long-term consequences.”

Molecules called free fatty acids circulating in the blood can directly increase the risk of diseases linked to obesity, according to a study released Wednesday by the journal Science Translational Medicine.

In addition, scientists at the Albert Einstein College of Medicine of New York and Southwestern Medical Center at the University of Texas said the study shows why dangerously inflamed fatty tissue in obese individuals.

The tissue inflammation is a normal process whereby the body tries to counteract the infection.

However, this can spin out in cases of obesity and diseases linked to overweight such as diabetes, cardiovascular diseases and some cancers.

According to scientists, the study clarifies the relationship between these fatty acids and inflammation in a breakthrough that could lead to development of better drugs for the treatment of patients with obesity-related diseases.

In the study, scientists administered a fatty acid group and no diabetic healthy adults in order to increase its presence at levels similar to those recorded in obesity and diabetes.

With such high levels of fatty acids, participants not only failed to respond properly to insulin, but also increased levels of a potentially harmful molecule, identified as PAI-1 and is believed to raise the risk factors for diabetes and cardiovascular diseases .

After examining the fabric of those participants, the researchers found that inflammatory cells congregate around the fatty tissue in obese people produced more PAI-1 molecules.

According to scientists, the presence of free fatty acids triggered inflammatory cells so therefore increasing the production of PAI-1.

Even in those with priorc drugs called inhibitors, proton pump can causes

Even in those with prior symptoms of heartburn drugs called inhibitors, proton pump can cause those symptoms once treatment is stopped, concludes a study published in the journal Gastroenterology.

“It seems that the drugs induce the symptoms they treat, which would generate” dependence on these drugs, told Reuters Health the study co-author Dr. Christina Reimer, University Hospital Koge, Denmark. This dependence may explain the increased use of these drugs.

Reimer’s team studied 120 healthy volunteers who received placebo treatment for 12 weeks or eight weeks regime inhibitor esomeprazole, proton pump plus four weeks of placebo pills.

Almost half (44 percent) of participants who had no heartburn symptoms developed clinically significant upon discontinuation of therapy between the ninth and twelfth week, unlike the 15 percent of placebo-treated group only.

The drugs are given to large numbers of patients, many of whom do not have symptoms associated with heartburn, said Reimer.

“The findings challenge the liberal policy of limitation and show that, as physicians, we should be more restrictive,” said the expert.

The authors of an editorial on the study agree. “We must work to limit the use of inhibitors of proton pump patients who will benefit from therapy,” write Drs Kenneth E. L. McColl and Derek Gillen, University of Glasgow in the UK.

In people who eat lots of red meat, cooked with some oil and use some types of polyunsaturated fatty acids and margarine heavy, increase the risk of inflammatory bowel disease, according to a study of more than 200,000 Europeans.

These foods are rich in linoleic acid and the study found that people more omega-6 polyunsaturated fatty acids consumed were twice as likely to develop ulcerative colitis.

The team of Dr. Andrew Hart of the University of East Anglia in Britain, also found that consuming more eicosapentaenoic acid, an omega-3 fatty acid in fish and fish oil was associated with a reduced risk of disease.

While the body needs a certain amount of linoleic acid to survive, as stated Hart told Reuters Health, the excess accumulates in the lining of the colon and, if released, it induces inflammation.

The omega-3 fatty acid does the opposite: “It inhibits inflammation,” he said.

To investigate the relationship between fatty acids and ulcerative colitis, which is chronic inflammation of the lining of the intestine, the team analyzed data from the European Prospective Investigation into essay Cancer and Nutrition (EPIC), which includes more than half a million people 10 European countries.

The analysis included 203,193 men and women, between 30 and 74. Within two to 11 years of follow up, 126 people developed ulcerative colitis.

Those in the highest quartile of intake of linoleic acid (13 to 38 grams daily) were 2.5 times more likely to have developed the disease than people who consumed just being 2 to 8 grams per day.

There is no effective treatment for food ulcerative colitis, Hart said, but the results raise the possibility that a diet low in linoleic acid may be useful.

According to Hart, a Mediterranean dietary pattern rich in fruits, vegetables and nut oil, would be reduced in linoleic acid and rich in omega 3. The researcher found that if omega-3s prevent ulcerative colitis, eating a couple servings of fish per week provide protection.

In people who eat lots of red meat, cooked with some oil and use some types of polyunsaturated fatty acids and margarine heavy, increase the risk of inflammatory bowel disease, according to a study of more than 200,000 Europeans.

These foods are rich in linoleic acid and the study found that people more omega-6 polyunsaturated fatty acids consumed were twice as likely to develop ulcerative colitis.

The team of Dr. Andrew Hart of the University of East Anglia in Britain, also found that consuming more eicosapentaenoic acid, an omega-3 fatty acid in fish and fish oil was associated with a reduced risk of disease.

While the body needs a certain amount of linoleic acid to survive, as stated Hart told Reuters Health, the excess accumulates in the lining of the colon and, if released, it induces inflammation.

The omega-3 fatty acid does the opposite: “It inhibits inflammation,” he said.

To investigate the relationship between fatty acids and ulcerative colitis, which is chronic inflammation of the lining of the intestine, the team analyzed data from the European Prospective Investigation into essay Cancer and Nutrition (EPIC), which includes more than half a million people 10 European countries.

The analysis included 203,193 men and women, between 30 and 74. Within two to 11 years of follow up, 126 people developed ulcerative colitis.

Those in the highest quartile of intake of linoleic acid (13 to 38 grams daily) were 2.5 times more likely to have developed the disease than people who consumed just being 2 to 8 grams per day.

There is no effective treatment for food ulcerative colitis, Hart said, but the results raise the possibility that a diet low in linoleic acid may be useful.

According to Hart, a Mediterranean dietary pattern rich in fruits, vegetables and nut oil, would be reduced in linoleic acid and rich in omega 3. The researcher found that if omega-3s prevent ulcerative colitis, eating a couple servings of fish per week provide protection.