The Administration of Escherichia coli Nissle 1917 Ameliorates Development of DSS-Induced Colitis in Mice
Metadatos
Mostrar el registro completo del ítemAutor
Rodríguez-Nogales, Alba; Algieri, Francesca; Garrido-Mesa, José; Vezza, Teresa; Utrilla, Maria P.; Chueca-Porcuna, Natalia; Fernández-Caballero, José Ángel; García García, Federico; Rodríguez Cabezas, María Elena; Gálvez Peralta, Julio JuanEditorial
Frontiers Media
Materia
Probiotic MicroRNA Pyrosequencing Intestinal microbiota DSS colitis
Fecha
2018-05-11Referencia bibliográfica
Rodríguez-Nogales A, Algieri F, Garrido-Mesa J, Vezza T, Utrilla MP, Chueca N, Fernández-Caballero JA, García F, Rodríguez-Cabezas ME and Gálvez J (2018) The Administration of Escherichia coli Nissle 1917 Ameliorates Development of DSS-Induced Colitis in Mice. Front. Pharmacol. 9:468. 10.3389/fphar.2018.00468.
Patrocinador
This work was supported by the Junta de Andalucía (CTS 164) and by the Spanish Ministry of Economy and Competitiveness (SAF2011-29648 and AGL2015-67995-C3-3-R) with funds from the European Union. The funders had no role in the study design, data collection, and analysis.Resumen
The beneficial effects of probiotics on immune-based pathologies such as inflammatory
bowel disease (IBD) have been well reported. However, their exact mechanisms have
not been fully elucidated. Few studies have focused on the impact of probiotics
on the composition of the colonic microbiota. The aim of the present study was
to correlate the intestinal anti-inflammatory activity of the probiotic Escherichia coli
Nissle 1917 (EcN) in the dextran sodium sulfate (DSS) model of mouse colitis with
the changes induced in colonic microbiota populations. EcN prevented the DSSinduced
colonic damage, as evidenced by lower disease activity index (DAI) values and
colonic weight/length ratio, when compared with untreated control mice. The beneficial
effects were confirmed biochemically, since the probiotic treatment improved the colonic
expression of different cytokines and proteins involved in epithelial integrity. In addition,
it restored the expression of different micro-RNAs (miR-143, miR-150, miR-155, miR-
223, and miR-375) involved in the inflammatory response that occurs in colitic mice.
Finally, the characterization of the colonic microbiota by pyrosequencing showed that
the probiotic administration was able to counteract the dysbiosis associated with the
intestinal inflammatory process. This effect was evidenced by an increase in bacterial
diversity in comparison with untreated colitic mice. The intestinal anti-inflammatory
effects of the probiotic EcN were associated with an amelioration of the altered
gut microbiome in mouse experimental colitis, especially when considering bacterial
diversity, which is reduced in these intestinal conditions. Moreover, this probiotic has
shown an ability to modulate expression levels of miRNAs and different mediators of the
immune response involved in gut inflammation. This modulation could also be of great
interest to understand the mechanism of action of this probiotic in the treatment of IBD.