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This article is the original of Translational Medicine Network, please indicate the source of reprinting
By Jevin
Researchers at Harvard Medical School analyzed molecular crosstalk
between pain fibers in the gut and goblet cells that line the intestinal wall.
This work shows that chemical signals from pain neurons induce goblet cells to release protective mucus to cover the intestine and protect it from damage
.
The findings suggest that intestinal pain is not a simple detection and signaling system, but plays a direct protective role
in the gut.
Recently, researchers from Harvard Medical School, the University of Chicago and the University of Gothenburg in Sweden found that pain neurons, nociceptive neurons, in the intestines of mice normally regulate the presence of protective mucus and stimulate intestinal cells to release more mucus in an inflammatory state
.
The study, published online in Cell on October 14, 2022, details the steps of
a complex signaling cascade.
style="box-sizing: border-box;" _msthash="251139" _msttexthash="275587">Receptor for RAMP1
01
The human intestines and respiratory tract are covered with goblet cells
.
Goblet cells, named for their goblet appearance, contain a gelatinous mucus composed of proteins and sugars that act as a protective coating that protects the surface of the organ from abrasion and damage
.
New research has found that when triggered by direct interaction with pain neurons in the gut, intestinal goblet cells release protective mucus
.
In one set of experiments, the researchers observed that mice lacking pain neurons produced less protective mucus and their gut microbial composition changed—the beneficial and harmful microbes in the gut were out of balance
.
To explain this phenomenon, they found that the surface of goblet cells contains a receptor called RAMP1, ensuring that these cells can respond to neighboring pain neurons that are activated
by dietary and microbial signals as well as mechanical stress, chemical stimulation, or drastic changes in temperature.
The experiment further showed that this receptor binds
to a chemical called CGRP released by neighboring pain neurons when stimulated.
They found that RAMP1 receptors were also present in human and mouse goblet cells, allowing them to respond to
pain signals.
The study further pointed out that the presence of certain gut microbes activates the release of CGRP to maintain the balance
of the gut.
Key promoter molecule CGRP
02
In addition to this, dietary factors also play a role
in activating pain receptors.
When the researchers gave capsaicin to mice, the mice's pain neurons were rapidly activated, causing the goblet cells to release large amounts of protective mucus
.
In contrast, mice lacking pain neurons or goblet cell CGRP receptors were more likely to develop colitis
.
This finding may explain why people with dysbiosis may be more likely to develop colitis
.
When the researchers injected mice lacking pain neurons with CGRP, which conducts pain signals, their mucus secretion improved
rapidly.
Even in the absence of painful neurons, this treatment protects mice from colitis
.
This finding suggests that CGRP is a key promoter
of the signaling cascade leading to protective mucus secretion.
Possible drawbacks of suppressing pain
03
The experiment showed that mice lacking pain receptors also suffered more severe damage
when colitis occurred.
Given that painkillers are often used to treat colitis patients, it may be important
to consider the possible adverse consequences of blocking pain, they said.
In people with intestinal inflammation, one of the main symptoms is pain, and some parts of this pain signal may act directly as a nerve reflex to protect it
.
In addition, the researchers say a class of common migraine drugs that inhibit CGRP secretion may damage intestinal barrier tissue
by interfering with this protective pain signal.
Resources:
style="white-space: normal;box-sizing: border-box;">Note: This article is intended to introduce the progress of medical research and cannot be used as a reference
for treatment options.
If you need health guidance, please go to a regular hospital
.
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