Article
Results from a mouse model study suggest that altering host gut microbiota via antibiotic treatment may reduce inflammation and other pathologies caused by H. pylori.
Researchers at the University of California, Santa Cruz, recently reported that the composition of the microbe population in the gut can have a significant influence on response to H. pylori in infected mice.
According to a news release from the American Society for Microbiology (ASM), “mice with different naturally occurring stomach bacteria have distinct susceptibilities to disease caused by Helicobacter pylori, the well-known cause of ulcers in humans.”
Karen Ottemann, PhD, and colleagues treated one group of mice with antibiotics, altering their gut microbiota, gave the same antibiotics to another group but then also fed them “normal stomach bacteria,” and left a third group of mice untreated.
The researchers observed that the mice treated with antibiotics had only small quantities of inflammatory Th1 T helper cells, whereas the untreated mice and the mice who received normal stomach bacteria had higher levels, suggesting that “the normal stomach microbes contribute to disease caused by H. pylori,” said Otteman.
Mice treated with antibiotics also had higher levels of inflammation-preventing Clostridia bacteria.
The study results were published in Infection and Immunity in an article titled “The Degree of Helicobacter Pylori Inflammation Is Manipulated by the Pre-Infection Host Microbiota.” In the article, the authors wrote that treating mice with antibiotics prior to infection with H. pylori “reduced CD4+ T-helper cells and Ifnγ transcript in gastric tissue after H. pylori infection. The bacterial communities in mice with a reduced response to H. pylori displayed many differences when compared to untreated mice, including significantly more cluster IV and XIVa Clostridium spp., bacteria known to influence inflammation via regulatory T cell populations.”
According to the authors, these findings “suggest that microbiota composition, perhaps Clostridium spp., contributes to the variable disease outcome of H. pylori infection by altering the recruitment of CD4+ T cells to the gastric compartment.” They also suggest that “gastric microbiota could be used as a diagnostic tool to determine which patients are at risk for developing severe disease.”
In the ASM news release, Otteman said that after additional investigations reveal “which microbes underlie H. pylori disease outcomes, we could test whether H. pylori-infected people harbor those particular bacteria, and target them for curing.”