Scientists have discovered unexpected protective properties of pain

(ORDO NEWS) — It turned out that gut pain neurons not only warn the brain of danger, but themselves protect the intestines from damage by forcing cells to produce more protective mucus.

Therefore, in the treatment of patients with inflammatory bowel diseases, according to scientists, one should be wary of painkillers.

Pain is a reliable warning system for damage to the body. But now, scientists from Harvard Medical School (USA) have shown that pain is more than just a signal: it is an independent form of protection.

The researchers found that pain neurons in the gut of mice regulate the secretion of protective mucus to goblet cells, both under normal conditions and during inflammation.

The intestine contains many goblet cells. These are secretory epithelial cells, named for their shape.

They contain a gel-like mucus composed of proteins and sugars that acts as a protective coating that keeps the intestines from being abraded and damaged.

A new study has shown that goblet cells secrete mucus by interacting directly with pain-sensitive gut neurons.

In a series of experiments, scientists observed how the intestines of mice devoid of pain neurons produced less mucus, which led to dysbacteriosis.

To find out how these disorders occur, the authors analyzed the properties of goblet cells in the presence and absence of pain neurons.

It turned out that RAMP1 receptors are located on the surface of goblet cells, which provide them with a connection with pain neurons.

Pain neurons are activated by substances found in food, intestinal bacteria, mechanical stress, or temperature changes.

With this stimulation, pain neurons release CGRP signaling molecules that interact with RAMP1 on the surface of goblet cells, which in turn begin to produce more mucus.

The presence of certain gut bacteria activates the release of CGRP to maintain gut homeostasis. Thus, pain neurons work not only during inflammation, but also in the normal state.

Mice that lacked pain neurons or goblet cell receptors were more susceptible to colitis, a form of inflammation of the intestinal mucosa.

This finding may explain why people with gut dysbiosis are more likely to experience the disease.

When the researchers injected CGRP into mice that lacked pain neurons, the animals experienced a rapid improvement in mucus production.

The treatment protected even subjects without pain neurons from colitis.

Given that pain medications are often used to treat patients with inflammatory bowel disease, it’s critical to consider the potential detrimental effects of blocking pain, scientists say.

In addition, the researchers stated that some common migraine medications that inhibit CGRP secretion may also damage intestinal tissues.

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