ACCORDING TO STUDIES, GUT NEURONS THAT SENSE PAIN HAVE ANTI-INFLAMMATORY PROPERTIES.

ACCORDING TO STUDIES, GUT NEURONS THAT SENSE PAIN HAVE ANTI-INFLAMMATORY PROPERTIES. IN TWO RECENT INVESTIGATIONS, PAIN-SENSING NEURONS IN THE STOMACH WERE FOUND TO FUNCTION AS MORE THAN MERELY SENSORY ALARM SYSTEMS, AS DESCRIBED IN THE JOURNAL CELL. 

ACCORDING TO THE FINDINGS, THESE NEURONS CAN DIRECTLY PREVENT INFLAMMATORY DAMAGE TO THE STOMACH.

OVERVIEW OF GUT NEURONS THAT SENSE PAIN HAVE ANTI-INFLAMMATORY PROPERTIES:

GUT NEURONS THAT SENSE PAIN HAVE ANTI-INFLAMMATORY PROPERTIES
GUT NEURONS THAT SENSE PAIN HAVE ANTI-INFLAMMATORY PROPERTIES

ACCORDING TO ISAAC CHIU, SENIOR RESEARCHER ON ONE OF THE TWO NEW STUDIES, “IT TURNS OUT THAT PAIN MAY PROTECT US IN MORE DIRECT WAYS THAN ITS CONVENTIONAL FUNCTION TO IDENTIFY POTENTIAL DAMAGE AND DISPATCH SIGNALS TO THE BRAIN.”

CHIU’S RESEARCH, DONE IN COLLABORATION WITH A GROUP FROM HARVARD MEDICAL SCHOOL, CONCENTRATED ON HOW PAIN NEURONS IN THE STOMACH CONNECT WITH GOBLET CELLS, A KIND OF CELL THAT LINING THE INTESTINES AND SECRETES PROTECTIVE MUCUS IN THE PRESENCE OF INFLAMMATION. 

ALTHOUGH IT WAS ASSUMED THAT THESE PAIN-SENSING NEURONS MUST SOMEHOW ALERT OTHER GUT CELLS TO DANGERS, RESEARCHERS WERE UNSURE OF THE PRECISE METHODS BY WHICH THIS OCCURRED UNTIL RECENTLY.

RESEARCHERS FROM HARVARD UNIVERSITY FOUND THAT GOBLET CELLS HAVE PARTICULAR RECEPTORS THAT CAN RECOGNISE SIGNALS PROVIDED BY PAIN NEURONS. 

CALCITONIN GENE-RELATED PEPTIDE IS A SUBSTANCE THAT PAIN NEURONS RELEASE IN RESPONSE TO STIMULATION (CGRP). AND IT APPEARS THAT THIS CHEMICAL SIGNAL IS A MAJOR CATALYST FOR GOBLET CELL MUCUS SECRETION.

THE RESEARCHERS SHOWED HOW CGRP PRODUCTION FROM PAIN NEURONS MAINTAINS OVERALL GUT HEALTH THROUGH A NUMBER OF MICE TESTS. IN ADDITION TO BEING ACTIVATED BY CGRP IN THE PRESENCE OF ACUTE INFLAMMATORY PAIN OR DAMAGE, GOBLET CELLS ALSO APPEARED TO BE ACTIVATED IN A HEALTHY GUT BY MICROORGANISMS AS A MEANS OF PRESERVING MICROBIOME BALANCE.

CHIU STATED, “THIS DATA SHOWS THAT THESE NERVES ARE STIMULATED NOT JUST BY ACUTE INFLAMMATION, BUT EVEN AT BASELINE.” THE MERE PRESENCE OF COMMON GUT MICROORGANISMS SEEMS TO IRRITATE THE NERVES AND TRIGGER THE RELEASE OF MUCUS FROM THE GOBLET CELLS.

THESE RESULTS HAVE THE COMPELLING IMPLICATION THAT SYSTEMIC SUPPRESSION OF A BODY’S PAIN RESPONSE MAY HAVE ADVERSE IMPACTS ON THIS DEFENCE MECHANISM.

RESEARCHERS OBSERVED MORE INFLAMMATORY DAMAGE IN ANIMALS DESIGNED TO EITHER LACK PAIN NEURONS IN THE STOMACH OR TO LACK CGRP RECEPTORS.

DISCOMFORT IS A COMMON INDICATION OF GUT INFLAMMATION, SO IT SEEMS SENSE THAT TREATING AND BLOCKING PAIN WOULD HELP PATIENTS FEEL BETTER, ACCORDING TO CHIU. 

HOWEVER, A PORTION OF THIS PAIN SIGNAL MAY ACTUALLY BE DIRECTLY PROTECTIVE AS A NEURONAL REACTION, RAISING SIGNIFICANT CONCERNS ABOUT HOW TO CAREFULLY CONTROL PAIN IN A WAY THAT DOES NOT RESULT IN ADDITIONAL DAMAGES.

ANOTHER JUST-PUBLISHED STUDY ALSO FOUND A NOVEL PROTECTIVE ROLE FOR PAIN-SENSING GUT NEURONS, THIS TIME BY RESEARCHERS AT WEILL CORNELL MEDICINE. THE GUT NERVES THAT CONTAIN THE TRPV1 RECEPTOR WERE THE SUBJECT OF THIS STUDY.

THE BRAIN REACTS TO THE STIMULATION OF TRPV1 RECEPTORS ON GUT NEURONS BY PRODUCING A BURNING TYPE OF ABDOMINAL PAIN THAT ANYONE WITH AN INFLAMMATORY BOWEL ILLNESS WOULD BE FAMILIAR WITH. 

THE RESEARCHERS DISCOVERED THAT TOTALLY SUPPRESSING TRPV1 RECEPTORS IN MICE MODELS INCREASED GUT INFLAMMATION, WHICH IS SOMEWHAT COUNTERINTUITIVE.

IT WAS NOW EVIDENT THAT THIS PAIN-SENSING RESPONSE WAS CARRYING OUT ADDITIONAL FUNCTIONS IN ADDITION TO JUST RELAYING FEELINGS TO THE BRAIN. FURTHER MOUSE RESEARCH DEMONSTRATED THAT THE LARGE ALTERATIONS IN GUT BACTERIAL POPULATIONS WERE RESPONSIBLE FOR THE ENHANCED INFLAMMATORY DAMAGE IN TRPV1-BLOCKED ANIMALS.

GUT NEURONS THAT SENSE PAIN HAVE ANTI-INFLAMMATORY PROPERTIES

IT TURNS OUT THAT TRPV1-EXPRESSING GUT NEURONS RELEASE SUBSTANCE P, A CHEMICAL THAT ENCOURAGES A BALANCED POPULATION OF BACTERIA IN THE STOMACH. MICE THAT HAD THEIR TRPV-1 BLOCKED COULD HAVE THEIR EFFECTS ON THEIR GUT MICROBES REVERSED BY ADMINISTERING THEM SUBSTANCE P DIRECTLY. 

ADDITIONALLY, THIS RESEARCH DISCOVERED THAT SOME BACTERIA MIGHT DIRECTLY ACTIVATE THE SECRETION OF SUBSTANCE P FROM GUT NERVES, JUST AS WAS SHOWN IN THE HARVARD STUDY WHEN BACTERIA WERE FOUND TO “TICKLE” GUT NERVES AND GENERATE THE RELEASE OF PROTECTIVE MUCOUS.

REGARDING THE FUNCTION OF GUT NEURONS IN INFLAMMATORY DISEASE, BOTH THESE RESEARCH UNDOUBTEDLY RAISE A NUMBER OF FRESH QUESTIONS. FOR INSTANCE, MAY THESE GUT NEURON PATHWAYS BE THE FOCUS OF FUTURE ANTI-INFLAMMATORY THERAPIES?

DAVID ARTIS, THE STUDY’S SENIOR AUTHOR, ASSERTS THAT THESE NEW DISCOVERIES OUGHT TO ALTER THE WAY WE VIEW INFLAMMATORY DISEASE.

MANY EXISTING ANTI-INFLAMMATORY MEDICATIONS ONLY BENEFIT SELECT INDIVIDUALS, AND PHARMACEUTICAL COMPANIES HAVEN’T REALLY FIGURED OUT WHY, ACCORDING TO ARTIS. “PERHAPS IT’S BECAUSE WE’VE ONLY BEEN SEEING A PORTION OF THE PICTURE WHEN IT COMES TO CHRONIC INFLAMMATION, AND NOW THE REST, INCLUDING THE NERVOUS SYSTEM’S PART, IS BEGINNING TO COME INTO FOCUS.”

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ACCORDING TO STUDIES, GUT NEURONS THAT SENSE PAIN HAVE ANTI-INFLAMMATORY PROPERTIES.

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