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Study links gut bacteria and lung infections
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Study links gut bacteria and lung infections

Gut microbiota plays an important role in improvising immunity in lungs and host’s defence against viral infection. A recent research focus upon lowering susceptibility to viral infection and their severity by reprogramming key immune cells present in the lungs.
Researchers has found that gut microbiota reduces the susceptibility to respiratory virus infection
Researchers has found that gut microbiota reduces the susceptibility to respiratory virus infection | Representative image Shutterstock

Researchers at the Institute of Biomedical Sciences at Georgia State University have found early evidence that the composition of the gut microbiota may play a role in determining how susceptible one is to viral lung infections. And how severely they may affect us.

In a study published in the journal Cell Host & Microbe, the researchers found that segmented filamentous bacteria (SFB) in mice — and also found in human intestines — safeguard against respiratory influenza virus.

They said that this protection was provided independent of whether these bacteria were naturally acquired or administered.

In their testing, the researchers saw that the protection offered by the bacteria was effective against respiratory syncytial virus (RSV) as well as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the main culprit behind the 2019 COVID pandemic.

They said the possible reason for this was that the bacteria could reprogramme immune cells present in the lungs (basally resident alveolar macrophages) to provide protection against the virus. These immune cells are the first responders against inhaled threats including viral infections.

Viral loads in the lungs

The study was conducted on mice, with specific differences in gut microbiota determined by the presence or absence of segmented filamentous bacteria or SFB. The animals were inoculated with respiratory influenza virus and the viral loads were assessed several days after infection. Mice with segmented filamentous bacteria showed a lower viral load than mice ones lacking the bacteria.

Similar results were obtained in animals infected with respiratory syncytial virus (RSV) and SARS-CoV-2.

Upon further investigation, they found that the alveolar macrophages were depleted in mice lacking the bacteria as the infection progressed. However, these immune cells were preserved in the animals having SFB.

Reprogrammed by gut microbiota

The researchers have found that there is an alteration in gene expression of these immune cells due to the presence of the bacteria that helped them to resist depletion. The macrophages eventually disable the virus by activating the immune complement against them.

Co-senior author of the study, Dr Andrew Ted Gewirtz, Regents’ Professor, Institute for Biomedical Sciences, Georgia State University, elaborated it in an email response to Happiest Health.

He said, “We hypothesise that segmented filamentous bacteria produce or induce production of metabolite(s) [travelling] to lungs to act on macrophages for causing these changes. We have some evidence that such molecules exist and [we] are trying to identify them.”

The finding, he said, may have uncovered a complex interaction between the microbes in our intestine and the immune cells in the lungs, determining the severity of respiratory infections.

Role in reducing infection

“We find it remarkable that the presence of a single bacterial species, amidst thousands of different microbial species inhabiting mouse gut, had such strong impacts in respiratory virus infection models,” said Dr Richard Plemper, co-senior author of the study, Regents’ Professor and director, Centre for Translational Antiviral Research, Georgia State University, in a statement.

He added that if the research findings are applicable to human infections, it could have major implications for the way we assess the risk of a person to developing severe lung infections. However, to establish this, a lot of work needs to be done.

Dr Gewirtz thinks it is highly unlikely that a single bacteria can alter the functionality of alveolar macrophages, and in turn lowering risk of someone developing respiratory viral infections.

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