The bacterium Helicobacter pylori that colonises the human stomach is now usually seen as a disease-causing organism. Pioneering research carried out by Barry J. Marshall and J. Robin Warren established infections by this bacterium as the most common cause of peptic ulcers.
Till their path-breaking work, for which they received the Nobel Prize in 2005, it had been believed that stress and lifestyle were responsible for producing such ulcers. Once the role played by H. pylori was recognised, eradicating it became the standard of care for ulcers where it was implicated. The bacterium was also found to be a major cause of stomach cancer.
However, H. pylori may not simply be a pathogen that is out to harm its human host.
“Helicobacter species may have been part of the indigenous gastric biota of humans and our prehuman ancestors from our earliest times,” remarked Martin Blaser of the New York University Langone Medical Center in the U.S. Such a long-standing relationship “suggests that benefits of H. pylori colonisation exist,” he noted in a journal paper published in 1998.
Large-scale studies had found that people without the bacterium were more likely to develop asthma, hay fever or skin allergies in childhood, he pointed out in a commentary, titled “Stop the killing of beneficial bacteria,” published in the journal Nature in 2011.
“And as H. pylori has disappeared from people’s stomachs, there has been an increase in gastroesophageal reflux, and its attendant problems such as Barrett’s oesophagus and oesophageal cancer. Could the trends be linked?”
Moreover, the bacterium does not always produce disease. Seven out of 10 Indians will have H. pylori infections, observed B.S. Ramakrishna, a gastroenterologist at the the SRM Institute of Medical Sciences in Chennai. But the vast majority do not have any symptoms of disease and only a small proportion develop ulcers.
A study carried out on mice suggests that other microbes present in the stomach could play a significant part in the inflammation set off by H. pylori.
The research, published in the journal Infection and Immunity, was motivated by the observation that identical mouse strains procured from different vendors responded differently when infected with the bacterium. Exploring further what caused this difference, Annah S. Rolig of the University of California at Santa Cruz and her colleagues found that mice with high levels of Clostridia bacteria in their stomach displayed low inflammation when infected with H. pylori.
Clostridia were known to prevent inflammation in the intestine and thus maybe key to dampening H. pylori pathology, although that remained to be determined, said Karen Ottemann, the principal investigator of the study, in a press release.
Variations in the microbes of the stomach could have “a dramatic effect on H. pylori-associated disease, and suggest new avenues for curbing H. pylori inflammation-related diseases such as ulcers and gastric cancer,” the scientists observed in their paper. However, “studies still need to be done in humans — right now, we do not know whether the findings apply to humans,” said Dr. Ottemann in an email.