Diesel exhaust particles (DEPs) are common airborne ultrafine particles (UFPs); however， few studies have examined their effects on the gastrointestinal tract. To investigate the interaction of gut microbiota and DEPs-induced colonic injury， adult C57BL/6 mice are kept in whole-body inhalation chambers and exposed to filtered room air (FRA) or DEPs (300 µg m) 1 h per day for 28 consecutive days. DEPs exposure results in colon epithelial injury with inflammatory cell infiltration and mucus depletion. Abundance of in murine feces is transiently increased following 7-day DEPs exposure and then decreased until the end of 28-day exposure. A reduction of the colonic mucus layer thickness is observed in mice rec... More
Diesel exhaust particles (DEPs) are common airborne ultrafine particles (UFPs); however， few studies have examined their effects on the gastrointestinal tract. To investigate the interaction of gut microbiota and DEPs-induced colonic injury， adult C57BL/6 mice are kept in whole-body inhalation chambers and exposed to filtered room air (FRA) or DEPs (300 µg m) 1 h per day for 28 consecutive days. DEPs exposure results in colon epithelial injury with inflammatory cell infiltration and mucus depletion. Abundance of in murine feces is transiently increased following 7-day DEPs exposure and then decreased until the end of 28-day exposure. A reduction of the colonic mucus layer thickness is observed in mice receiving gut microbiota from DEPs-exposed mice. Mechanistically， RNA-sequencing suggests disruption of the nitrogen metabolism pathway in DEPs-exposed NCM460 cells. Upregulation of carbonic anhydrase 9 (CA9) expression levels is observed in epithelia following DEPs exposure both in vivo and in vitro. Oral administration of probiotics protects the mice against DEPS-induced colon epithelial injury. The results strongly suggest the involvement of gut microbiota in response to DEPs exposure and subsequently epithelial injury in vivo. Supplementation with probiotic may be a potential way to protect against UFPs-induced colon epithelial injury.
