4.7 Article

Probiotic lactobacilli as a promising strategy to ameliorate disorders associated with intestinal inflammation induced by a non-steroidal anti-inflammatory drug

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SCIENTIFIC REPORTS
卷 11, 期 1, 页码 -

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NATURE RESEARCH
DOI: 10.1038/s41598-020-80482-z

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  1. Agencia Nacional de Promocion Cientifica y Tecnica (PICT) [2964]
  2. Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET) [PIP 806]
  3. Universidad Nacional de Tucuman [PIUNT D624]

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Probiotic supplementation can reduce symptoms of NSAID-induced inflammation in the small intestine, increase antimicrobial activity in the intestines, and promote changes in the gut microbiota to maintain intestinal homeostasis.
Damage to the small intestine caused by non-steroidal anti-inflammatory drugs (NSAIDs) occurs more frequently than in the upper gastrointestinal tract, is more difficult to diagnose and no effective treatments exist. Hence, we investigated whether probiotics can control the onset of this severe condition in a murine model of intestinal inflammation induced by the NSAID, indomethacin. Probiotic supplementation to mice reduce the body weight loss, anemia, shortening of the small intestine, cell infiltration into the intestinal tissue and the loss of Paneth and Goblet cells associated with intestinal inflammation. Furthermore, a high antimicrobial activity in the intestinal fluids of mice fed with probiotics compared to animals on a conventional diet was elicited against several pathogens. Interestingly, probiotics dampened the oxidative stress and several local and systemic markers of an inflammatory process, as well as increased the secretion of IL-10 by regulatory T cells. Even more importantly, probiotics induced important changes in the large intestine microbiota characterized by an increase in anaerobes and lactobacilli, and a significant decrease in total enterobacteria. We conclude that oral probiotic supplementation in NSAID-induced inflammation increases intestinal antimicrobial activity and reinforces the intestinal epithelial barrier in order to avoid pathogens and commensal invasion and maintain intestinal homeostasis.

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