Do oral and gut microbiota communicate through redox pathways? A novel asset of the nitrate‐nitrite‐NO pathway
Nitrate may act as a regulator of •NO bioavailability via sequential reduction along the nitrate‐nitrite‐NO pathway with widespread health benefits, including a eubiotic effect on the oral and gut microbiota. Here, we discuss the molecular mechanisms of microbiota‐host communication through redox pa...
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Published in | FEBS letters Vol. 598; no. 17; pp. 2211 - 2223 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
England
01.09.2024
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Subjects | |
Online Access | Get full text |
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Summary: | Nitrate may act as a regulator of •NO bioavailability via sequential reduction along the nitrate‐nitrite‐NO pathway with widespread health benefits, including a eubiotic effect on the oral and gut microbiota. Here, we discuss the molecular mechanisms of microbiota‐host communication through redox pathways, via the production of •NO and oxidants by the family of NADPH oxidases, namely hydrogen peroxide (via Duox2), superoxide radical (via Nox1 and Nox2) and peroxynitrite, which leads to downstream activation of stress responses (Nrf2 and NFkB pathways) in the host mucosa. The activation of Nox2 by microbial metabolites is also discussed. Finally, we propose a new perspective in which both oral and gut microbiota communicate through redox pathways, with nitrate as the pivot linking both ecosystems.
The oral and gut microbiotas are distinct microbial communities with unique compositions and functions but they can communicate and influence each other. Antibiotics disrupt the oral and gut ecosystems, leading to dysbiosis and increased gut epithelial permeability. Nitrate may promote inter‐kingdom crosstalk during dysbiosis by either generating redox signalling species or serving as a substrate for bacteria in both ecosystems. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
ISSN: | 0014-5793 1873-3468 1873-3468 |
DOI: | 10.1002/1873-3468.14859 |