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Inflammation-associated nitrate facilitates ectopic colonization of oral bacterium Veillonella parvula in the intestine

维管菌 生物 微生物学 炎症性肠病 结肠炎 炎症 细菌 内科学 免疫学 疾病 医学 遗传学 链球菌
作者
Daniel F. Rojas‐Tapias,Eric Brown,Emily R. Temple,Michelle A. Onyekaba,Ahmed Mohamed,Kellyanne Duncan,Melanie Schirmer,Rebecca L. Walker,Toufic Mayassi,Kerry A. Pierce,Julián Ávila-Pacheco,Clary B. Clish,Hera Vlamakis,Ramnik J. Xavier
出处
期刊:Nature microbiology [Nature Portfolio]
卷期号:7 (10): 1673-1685 被引量:82
标识
DOI:10.1038/s41564-022-01224-7
摘要

Colonization of the intestine by oral microbes has been linked to multiple diseases such as inflammatory bowel disease and colon cancer, yet mechanisms allowing expansion in this niche remain largely unknown. Veillonella parvula, an asaccharolytic, anaerobic, oral microbe that derives energy from organic acids, increases in abundance in the intestine of patients with inflammatory bowel disease. Here we show that nitrate, a signature metabolite of inflammation, allows V. parvula to transition from fermentation to anaerobic respiration. Nitrate respiration, through the narGHJI operon, boosted Veillonella growth on organic acids and also modulated its metabolic repertoire, allowing it to use amino acids and peptides as carbon sources. This metabolic shift was accompanied by changes in carbon metabolism and ATP production pathways. Nitrate respiration was fundamental for ectopic colonization in a mouse model of colitis, because a V. parvula narG deletion mutant colonized significantly less than a wild-type strain during inflammation. These results suggest that V. parvula harness conditions present during inflammation to colonize in the intestine. The oral bacterium Veillonella parvula utilizes inflammation-associated nitrate to facilitate colonization of the intestinal tract, which is observed in a mouse model of colitis and patients with inflammatory bowel disease.
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