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Nitrate from diet might fuel gut microbiota metabolism: Minding the gap between redox signaling and inter-kingdom communication.
Free Radic Biol Med. 2020 Mar; 149:37-43.FR

Abstract

The gut microbiota has been recently interpreted in terms of a metabolic organ that influences the host through reciprocal interactions, encompassing metabolic and immune pathways, genetic and epigenetic programming in host mammal tissues in a diet-depended manner, that shape virtually all aspects of host physiology. In this scenario, dietary nitrate, a major component of leafy green vegetables known for their health benefits, might fuel microbiota metabolism with ensued consequences for microbiota-host interaction. Cumulating evidence support that nitrate shapes oral microbiome communities with impact on the kinetics and systemic levels of both nitrate and nitrite. However, the impact of nitrate, which is steadily delivered into the lower gastrointestinal tract after a vegetable-rich meal, in the intestinal microbiome communities and their functional capacity remains largely elusive. Several mechanisms reinforce the notion that nitrate may be a nutrient for the lower microbiome and might participate in local redox interactions with relevance for bacteria-host interactions, among these nitric oxide-dependent mechanisms along the nitrate-nitrite-nitric oxide pathway. Also, by allowing bacteria to thrive, either by increasing microbial biomass or by acting as a respiratory substrate for the existing communities, nitrate ensures the production of bacterial metabolites (e.g., pathogen-associated molecular patterns, PAMP, short chain fatty acids, among other) that are recognised by host receptors (such as toll-like, TLR, and formyl peptide receptors, FPR) thereby activating local signalling pathways. Here, we elaborate on the notion that via modulation of intestinal microbiota metabolism, dietary nitrate impacts on host-microbiota metabolic and redox interactions, thereby contributing as an essential nutrient to optimal health.

Authors+Show Affiliations

Faculty of Pharmacy and Center for Neuroscience and Cell Biology, University of Coimbra, Health Sciences Campus, Azinhaga de Santa Comba, 3000-548, Coimbra, Portugal. Electronic address: barbarasrocha@icloud.com.Faculty of Pharmacy and Center for Neuroscience and Cell Biology, University of Coimbra, Health Sciences Campus, Azinhaga de Santa Comba, 3000-548, Coimbra, Portugal.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

32045656

Citation

Rocha, Bárbara S., and João Laranjinha. "Nitrate From Diet Might Fuel Gut Microbiota Metabolism: Minding the Gap Between Redox Signaling and Inter-kingdom Communication." Free Radical Biology & Medicine, vol. 149, 2020, pp. 37-43.
Rocha BS, Laranjinha J. Nitrate from diet might fuel gut microbiota metabolism: Minding the gap between redox signaling and inter-kingdom communication. Free Radic Biol Med. 2020;149:37-43.
Rocha, B. S., & Laranjinha, J. (2020). Nitrate from diet might fuel gut microbiota metabolism: Minding the gap between redox signaling and inter-kingdom communication. Free Radical Biology & Medicine, 149, 37-43. https://doi.org/10.1016/j.freeradbiomed.2020.02.001
Rocha BS, Laranjinha J. Nitrate From Diet Might Fuel Gut Microbiota Metabolism: Minding the Gap Between Redox Signaling and Inter-kingdom Communication. Free Radic Biol Med. 2020;149:37-43. PubMed PMID: 32045656.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitrate from diet might fuel gut microbiota metabolism: Minding the gap between redox signaling and inter-kingdom communication. AU - Rocha,Bárbara S, AU - Laranjinha,João, Y1 - 2020/02/08/ PY - 2019/12/30/received PY - 2020/01/29/revised PY - 2020/02/03/accepted PY - 2020/2/12/pubmed PY - 2020/2/12/medline PY - 2020/2/12/entrez KW - Diet KW - Nitrate KW - Nitric oxide KW - Nitrite KW - Redox signalling KW - gut microbiota SP - 37 EP - 43 JF - Free radical biology & medicine JO - Free Radic. Biol. Med. VL - 149 N2 - The gut microbiota has been recently interpreted in terms of a metabolic organ that influences the host through reciprocal interactions, encompassing metabolic and immune pathways, genetic and epigenetic programming in host mammal tissues in a diet-depended manner, that shape virtually all aspects of host physiology. In this scenario, dietary nitrate, a major component of leafy green vegetables known for their health benefits, might fuel microbiota metabolism with ensued consequences for microbiota-host interaction. Cumulating evidence support that nitrate shapes oral microbiome communities with impact on the kinetics and systemic levels of both nitrate and nitrite. However, the impact of nitrate, which is steadily delivered into the lower gastrointestinal tract after a vegetable-rich meal, in the intestinal microbiome communities and their functional capacity remains largely elusive. Several mechanisms reinforce the notion that nitrate may be a nutrient for the lower microbiome and might participate in local redox interactions with relevance for bacteria-host interactions, among these nitric oxide-dependent mechanisms along the nitrate-nitrite-nitric oxide pathway. Also, by allowing bacteria to thrive, either by increasing microbial biomass or by acting as a respiratory substrate for the existing communities, nitrate ensures the production of bacterial metabolites (e.g., pathogen-associated molecular patterns, PAMP, short chain fatty acids, among other) that are recognised by host receptors (such as toll-like, TLR, and formyl peptide receptors, FPR) thereby activating local signalling pathways. Here, we elaborate on the notion that via modulation of intestinal microbiota metabolism, dietary nitrate impacts on host-microbiota metabolic and redox interactions, thereby contributing as an essential nutrient to optimal health. SN - 1873-4596 UR - https://www.unboundmedicine.com/medline/citation/32045656/Nitrate_from_diet_might_fuel_gut_microbiota_metabolism:_Minding_the_gap_between_redox_signaling_and_inter-kingdom_communication L2 - https://linkinghub.elsevier.com/retrieve/pii/S0891-5849(19)32603-6 DB - PRIME DP - Unbound Medicine ER -
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