Alanyl-glutamine Protects Against Damage Induced by Enteroaggregative Escherichia coli Strains in Intestinal Cells

Autor: Samilly A. Ribeiro, Mara M. G. Prata, Mayra A V Reyes, Richard L. Guerrant, Marco A F Clementino, Ila F. N. Lima, Roberto C. P. Lima-Júnior, Josiane da Silva Quetz, Paloma A. Cavalcante, Antonio Vinicios Alves da Silva, Eudmar M de Assis Júnior, Aldo A. M. Lima, Pedro H. Q. S. Medeiros, Alexandre Havt
Rok vydání: 2019
Předmět:
Zdroj: Journal of Pediatric Gastroenterology & Nutrition. 68:190-198
ISSN: 1536-4801
0277-2116
Popis: Background Enteroaggregative Escherichia coli (EAEC) is an important pathogen causing enteric infections worldwide. This pathotype is linked to malnutrition in children from developing countries. Alanyl-glutamine (Ala-Gln) is an immune modulator nutrient that acts during intestinal damage and/or inflammation. This study investigated the effect of EAEC infection and Ala-Gln on cell viability, cell death, and inflammation of intestinal epithelium cells (IEC-6). Methods Cells were infected with an EAEC prototype 042 strain, an EAEC wild-type strain isolated from a Brazilian malnourished child, and a commensal E coli HS. Gene transcription and protein levels of caspases-3, -8, and -9 and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL1) were evaluated using RT-qPCR, western blot analysis, and ELISA. Results Infections with both EAEC strains decreased cell viability and induced apoptosis and necrosis after 24 hours. Ala-Gln supplementation increased cell proliferation and reduced cell death in infected cells. Likewise, EAEC strain 042 significantly increased the transcript levels of caspases-3, -8, and -9 when compared to the control group, and Ala-Gln treatment reversed this effect. Furthermore, EAEC induced CXCL1 protein levels, which were also reduced by Ala-Gln supplementation. Conclusion These findings suggest that EAEC infection promotes apoptosis, necrosis, and intestinal inflammation with involvement of caspases. Supplementation of Ala-Gln inhibits cell death, increases cell proliferation, attenuates mediators associated with cell death, and inflammatory pathways in infected cells.
Databáze: OpenAIRE
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