‘Stomach-ache’ neurons rush to the rescue when bacteria invade

[Andy]

Nerve cells in the gut have a leading role in preventing a misery that afflicts millions of people every year: diarrhoea and vomiting caused by infection with Salmonella bacteria.

Nerve cells called nociceptors monitor the gut and, if they notice problems, trigger a defence response, such as stomach pain. To investigate these cells’ defensive powers, Isaac Chiu at Harvard Medical School in Boston, Massachusetts, and his colleagues bred mice missing one class of nociceptors. The team then infected the mice with the bacterium Salmonella enterica, a common cause of intestinal distress. One day later, the mice without nociceptors had nearly 100 times more bacteria in one portion of the gut than normal mice did.

https://www.nature.com/articles/d41586-019-03725-8

The paper itself: Gut-Innervating Nociceptor Neurons Regulate Peyer’s Patch Microfold Cells and SFB Levels to Mediate Salmonella Host Defense

Highlights

• Nociceptors mediate enteric defense against Salmonella colonization and PP invasion
• Nociceptors shape the gut microbiota and SFB levels to resist Salmonella infection
• Nociceptors suppress M cell density to regulate SFB and limit bacterial invasion
• Nociceptors directly sense Salmonella to release CGRP to promote host defense

Summary
Gut-innervating nociceptor sensory neurons respond to noxious stimuli by initiating protective responses including pain and inflammation; however, their role in enteric infections is unclear. Here, we find that nociceptor neurons critically mediate host defense against the bacterial pathogen Salmonella enterica serovar Typhimurium (STm). Dorsal root ganglia nociceptors protect against STm colonization, invasion, and dissemination from the gut. Nociceptors regulate the density of microfold (M) cells in ileum Peyer’s patch (PP) follicle-associated epithelia (FAE) to limit entry points for STm invasion. Downstream of M cells, nociceptors maintain levels of segmentous filamentous bacteria (SFB), a gut microbe residing on ileum villi and PP FAE that mediates resistance to STm infection. TRPV1+ nociceptors directly respond to STm by releasing calcitonin gene-related peptide (CGRP), a neuropeptide that modulates M cells and SFB levels to protect against Salmonella infection. These findings reveal a major role for nociceptor neurons in sensing and defending against enteric pathogens.

Paywall, https://www.cell.com/cell/fulltext/S0092-8674(19)31270-X
Sci hub, https://sci-hub.se/10.1016/j.cell.2019.11.014

 

[rvallee]

An interesting question would be how common it is to ingest a small number of not-particularly-vibrant salmonella bacteria (or any other that generate a similar nociceptive response) and whether this could be a rather common cause of digestive pain, whether there is a threshold that will not trigger a full evacuation but still lead to what some people would qualify as IBS or something like it. Especially considering how unfortunately common it is to find fecal bacteria and other types of nasties in food.

Depends of course on beliefs about pain, though, whether people who believe pain does not actually exist without injury have some thoughts and beliefs about what the salmonella are thinking, or something like that. Somehow I don't think either of the bacteria or the watchful neurons will be particularly receptive to CBT, then again I'm sure someone will come up with a way to make the case that, at the very least, more research is needed to figure out how to change the germs' bad behavior.