The intestinal epithelium separates host tissue and gut-associated microbial communities. During inflammation, the host releases reactive oxygen and nitrogen species as an antimicrobial response. The impact of these radicals on gut microbes is incompletely understood. We discovered that the cryptic appBCX genes, predicted to encode a cytochrome bd-II oxidase, conferred a fitness advantage for E. coli in chemical and genetic models of non-infectious colitis. This fitness advantage was absent in mice that lacked epithelial NADPH oxidase 1 (NOX1) activity. In laboratory growth experiments, supplementation with exogenous hydrogen peroxide enhanced E. coli growth through AppBCX-mediated respiration in a catalase-dependent manner. We conclude that epithelial-derived reactive oxygen species are degraded in the gut lumen, which gives rise to molecular oxygen that supports the aerobic respiration of E. coli. This work illustrates how epithelial host responses intersect with gut microbial metabolism in the context of gut inflammation.

肠上皮将宿主组织和肠道相关微生物群落分开。在炎症期间，宿主释放活性氧和氮物质作为抗菌反应。这些自由基对肠道微生物的影响尚不完全清楚。我们发现，预测编码细胞色素 bd-II 氧化酶的神秘appBCX基因在非传染性结肠炎的化学和遗传模型中为大肠杆菌赋予了适应性优势。这种适应性优势在缺乏上皮 NADPH 氧化酶 1 (NOX1) 活性的小鼠中不存在。在实验室生长实验中，补充外源性过氧化氢增强了大肠杆菌通过 AppBCX 介导的呼吸以过氧化氢酶依赖性方式生长。我们得出结论，上皮衍生的活性氧在肠腔中降解，从而产生支持大肠杆菌有氧呼吸的分子氧。这项工作说明了在肠道炎症的背景下上皮宿主反应如何与肠道微生物代谢相交。