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Probiotics Ameliorate Colon Epithelial Injury Induced by Ambient Ultrafine Particles Exposure
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 chamb...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6755525/ https://www.ncbi.nlm.nih.gov/pubmed/31559135 http://dx.doi.org/10.1002/advs.201900972 |
Sumario: | 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(−3)) 1 h per day for 28 consecutive days. DEPs exposure results in colon epithelial injury with inflammatory cell infiltration and mucus depletion. Abundance of Lactobacillus 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. |
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