How does gut bacteria maintain its stability during inflammation?

The human gut (intestine) has a dynamic ecosystem consisting of bacteria which can be either beneficial or harmful to the body. These microbial colonies are key to proper digestive functioning and it is noteworthy to understand how they have evolved to withstand bodily disruptions such as dietary changes, pathogens and toxin exposure.

The body responds to infection by activating its inflammatory mechanisms and by secreting molecules likeantimicrobial peptides (AMPs) which kill harmful bacteria. In spite of that, healthy gut microbial communities can resist AMPs and can remain stable for years in the gut.

The mechanism by which, these gut micro-organisms or microbiota can withstand high levels of inflammation-associated anti-microbial peptides (AMPs), was studied in a paper published in the journal ‘Science’. They studied a prominent gut commensal (a harmless co-existing bacteria), Bacteroides thetaiotaomicron which underwent a liposaccharide modification on its surface, allowing it to resist mammalian AMPs effectively.

Moreover, mass spectroscopy experiments revealed the presence of a specific phosphate group which alters the surface charge of the bacteria and neutralizes the negative charge of the cell, thereby decreasing antimicrobial binding. The protein responsible for this was identified as LpxF. Mutant bacteria in which this particular phosphate group was removed became more susceptible to AMP.

This gut microflora performs various useful functions for the host, such as fermenting unused energy substrates, preventing growth of harmful pathogenic bacteria and producing vitamins such as biotin and Vitamin K. A major factor in health is the balance of bacterial numbers; if the numbers are too high or low, it will result in harm to the host. Thus, understanding the mechanisms which are responsible for their stability is crucial, so that we can manipulate these communities for therapeutic purposes.

The original publication can be accessed here.