HUMAN INTESTINAL MICROBIOTA IS CHARACTERIZED BY HIGH POPULATION DENSITY, WIDE DIVERSITY AND COMPLEXITY OF INTERACTIONS. DYSBIOSIS, BOTH QUALITATIVE AND QUANTITATIVE, MIGHT HAVE SERIOUS HEALTH CONSEQUENCES INCLUDING AN INCREASE IN THE NUMBER AND/OR ALTERATION OF BACTERIAL COLONIZING THE GASTROINTESTINAL TRACT, WHICH COULD BE REFERRED AS GUT MICROFLORA IMBALANCE (GMI). GMI IS FREQUENTLY FIUND IN PATIENTS SUFFERING FROM IRRITABLE BOWEL SYNDROME; THIS IS THE REASON WHY SOME AUTHORS BELIEVE THAT IBS IS SECONDARY TO GMI. INTERESTINGLY, GMI IS ALSO FOUND IN ABOUT 25% OF CROHN'S DISEASE PATIENTS. STIMULATION OF INFLAMMATION BY THE DANGEROUS BACTERIA, THROUG SPECIFIC ACTIVATION OF THE INTESTINAL IMMUNE SYSTEM, SEEMS TO BE THE WIDELY ACCEPTED PATHOGENETIC HYPOTHESIS TO EXPLAIN SUCH A CORRELATION; ON THE CONTRARY, SOME COMPONENTS OF THE INTESTINAL MICROFLORA COULD ALSO EXERT A PROTECTIVE ROLE THROUGH IMMUNOMODULATION. STIMULATION OF INFLAMMATION IS ALSO THE MAIN MECHANISM BY WHICH THE GUT MICROFLORA COULD INCREASE THE CANCER RISK; ANOTHER ALTERNATIVE, BUT NOT MUTUALLY EXCLUSIVE, PATHOGENIC HYPOTHESIS INVOLVES THE REGULATION OF PROLIFERATION/DIFFERENTATION OF INTESTINAL STEM CELLS. IN THIS REVIEW, SOME INTERESTING DATA REGARDING BIOMOLECULAR ALTERATIONS ASSOCIATED WITH INTESTINAL BOWEL DISEASES WILL BE DESCRIBED. WE WILL DISCUSS MORE RECENT, FINDINGS ABOUT THE RELATIONSHIP BETWEEN GMI AND INTESTINAL CHRONIC INFLAMMATION, POINTING OUT THE ONCOGENIC RISK RELATED TO ALTERATION OF MICROBIOTA COMPOSITION. FINALLY, WE GENERATE AN INTRIGUING HYPOTHESIS REGARDING A NETWORK BETWEEN GUT MICROFLORA AND INTESTINAL STEM CELLS.

Tomasello, G., Bellavia, M., Damiano, G., Gioviale, M.C., Lo Monte AI (2012). POSSIBLE RELATION BETWEEN GUT MICROFLORA COMPOSITION AND ONCOGENIC RISK: IS STIMULATION OF INFLAMMATION THE ONE RING OF CONNECTION?. REVIEWS IN MEDICAL MICROBIOLOGY, 23, 52-57 [10.1097/MRM.obo13e328353f49c].

POSSIBLE RELATION BETWEEN GUT MICROFLORA COMPOSITION AND ONCOGENIC RISK: IS STIMULATION OF INFLAMMATION THE ONE RING OF CONNECTION?

TOMASELLO, Giovanni;Damiano, G;GIOVIALE, Maria Concetta;LO MONTE, Attilio Ignazio
2012-01-01

Abstract

HUMAN INTESTINAL MICROBIOTA IS CHARACTERIZED BY HIGH POPULATION DENSITY, WIDE DIVERSITY AND COMPLEXITY OF INTERACTIONS. DYSBIOSIS, BOTH QUALITATIVE AND QUANTITATIVE, MIGHT HAVE SERIOUS HEALTH CONSEQUENCES INCLUDING AN INCREASE IN THE NUMBER AND/OR ALTERATION OF BACTERIAL COLONIZING THE GASTROINTESTINAL TRACT, WHICH COULD BE REFERRED AS GUT MICROFLORA IMBALANCE (GMI). GMI IS FREQUENTLY FIUND IN PATIENTS SUFFERING FROM IRRITABLE BOWEL SYNDROME; THIS IS THE REASON WHY SOME AUTHORS BELIEVE THAT IBS IS SECONDARY TO GMI. INTERESTINGLY, GMI IS ALSO FOUND IN ABOUT 25% OF CROHN'S DISEASE PATIENTS. STIMULATION OF INFLAMMATION BY THE DANGEROUS BACTERIA, THROUG SPECIFIC ACTIVATION OF THE INTESTINAL IMMUNE SYSTEM, SEEMS TO BE THE WIDELY ACCEPTED PATHOGENETIC HYPOTHESIS TO EXPLAIN SUCH A CORRELATION; ON THE CONTRARY, SOME COMPONENTS OF THE INTESTINAL MICROFLORA COULD ALSO EXERT A PROTECTIVE ROLE THROUGH IMMUNOMODULATION. STIMULATION OF INFLAMMATION IS ALSO THE MAIN MECHANISM BY WHICH THE GUT MICROFLORA COULD INCREASE THE CANCER RISK; ANOTHER ALTERNATIVE, BUT NOT MUTUALLY EXCLUSIVE, PATHOGENIC HYPOTHESIS INVOLVES THE REGULATION OF PROLIFERATION/DIFFERENTATION OF INTESTINAL STEM CELLS. IN THIS REVIEW, SOME INTERESTING DATA REGARDING BIOMOLECULAR ALTERATIONS ASSOCIATED WITH INTESTINAL BOWEL DISEASES WILL BE DESCRIBED. WE WILL DISCUSS MORE RECENT, FINDINGS ABOUT THE RELATIONSHIP BETWEEN GMI AND INTESTINAL CHRONIC INFLAMMATION, POINTING OUT THE ONCOGENIC RISK RELATED TO ALTERATION OF MICROBIOTA COMPOSITION. FINALLY, WE GENERATE AN INTRIGUING HYPOTHESIS REGARDING A NETWORK BETWEEN GUT MICROFLORA AND INTESTINAL STEM CELLS.
2012
Tomasello, G., Bellavia, M., Damiano, G., Gioviale, M.C., Lo Monte AI (2012). POSSIBLE RELATION BETWEEN GUT MICROFLORA COMPOSITION AND ONCOGENIC RISK: IS STIMULATION OF INFLAMMATION THE ONE RING OF CONNECTION?. REVIEWS IN MEDICAL MICROBIOLOGY, 23, 52-57 [10.1097/MRM.obo13e328353f49c].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10447/67643
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