Researchers have indicated that infection with the gastric bacterium Helicobacter pylori provides reliable protection against allergy-induced asthma.
The results confirmed the hypothesis recently put forward that the dramatic increase in allergic diseases in industrial societies is linked to the rapid disappearance of specific micro-organisms that populate the human body.
Scientists from the University of Zurich and the University Medical Center of the Johannes Gutenberg University Mainz have now revealed that the increase in asthma could be put down to the specific disappearance of the gastric bacterium Helicobacter pylori (H. pylori) from Western societies.
Asthma
H. pylori is resistant to gastric acid. The affliction often has no symptoms, but under certain conditions can cause gastritis, gastric and duodenal ulcers, and stomach cancer. Consequently, H. pylori is often killed off with antibiotics as a precaution, even if the patient does not have any complaints.
For their study, the researchers infected mice with H. pylori bacteria. If the mice were infected at the age of a few days old, they developed immunological tolerance to the bacterium and even reacted insignificantly – if at all – to strong, asthma-inducing allergens. Mice that were not infected with H. pylori until they had reached adulthood, however, had a much weaker defence.
“Early infection impairs the maturation of the dendritic cells and triggers the accumulation of regulatory T-cells that are crucial for the suppression of asthma,” said Anne Muller, a professor of molecular cancer research at the University of Zurich, explaining the protective mechanism.
If regulatory T-cells were transferred from infected to uninfected mice, they too enjoyed effective protection against allergy-induced asthma. However, mice that had been infected early also lost their resistance to asthma-inducing allergens if H. pylori were killed off in them with the aid of antibiotics after the sensitisation phase.
The study has been published in the prestigious Journal of Clinical Investigation.
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A new study has established a link between a master molecule of the immune system to the pathology of asthma.
Researchers have revealed that gamma interferon”s role in asthma has been fuzzy. High levels of this substance in children”s blood seem to be protective against the development of the disease.
The key immune molecule has often been assumed to steer the immune system in a different direction from the cluster of allergic disorders to which asthma belongs.
Yet, studies have found that high gamma-interferon concentrations are frequently found in severe asthmatics” lungs.
“People thought gamma-interferon might have something to do with driving asthma”s pathology, but there wasn”t a whole lot of corroborating evidence,” said Stephen Galli, MD, professor and chair of the Department of Pathology at Stanford medical school.
According to the researchers, gamma-interferon, a signaling molecule secreted by certain immune cells mobilizes the immune system to fight infectious pathogens or to attack healthy tissues, resulting in autoimmune diseases.
They used a mouse model of asthma to pin down gamma-interferon”s role in that disease.
The researchers provided mast-cell-deficient mice with mast cells whose surface receptors for gamma interferon had been knocked out.
It was seen that giving fully functioning mast cells to such mice restored the protocol”s power to trigger the asthma-associated symptoms and gene-activity level changes that normal mice develop under the regimen.
“This is potential important news, because it suggests that gamma-interferon might represent a therapeutic target,” said Galli.
The new study reproduced not only the gross symptoms of asthma in the mice, but also the overall patterns of changes in the activity of genes in lung tissue that typify people with asthma.
The study has been published online in the Journal of Clinical Investigation.