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Journal of Immunology Research
Volume 2017, Article ID 6976935, 9 pages
https://doi.org/10.1155/2017/6976935
Research Article

Beta-Defensin-2 and Beta-Defensin-3 Reduce Intestinal Damage Caused by Salmonella typhimurium Modulating the Expression of Cytokines and Enhancing the Probiotic Activity of Enterococcus faecium

Department of Experimental Medicine, University of Campania “Luigi Vanvitelli”, Via De Crecchio No. 7, 80138 Naples, Italy

Correspondence should be addressed to Alessandra Fusco; ti.ainapmacinu@ocsuf.ardnassela and Giovanna Donnarumma; ti.ainapmacinu@ammurannod.annavoig

Received 29 May 2017; Revised 9 August 2017; Accepted 5 September 2017; Published 9 November 2017

Academic Editor: Mitesh Dwivedi

Copyright © 2017 Alessandra Fusco et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The intestinal microbiota is a major factor in human health and disease. This microbial community includes autochthonous (permanent inhabitants) and allochthonous (transient inhabitants) microorganisms that contribute to maintaining the integrity of the intestinal wall, modulating responses to pathogenic noxae and representing a key factor in the maturation of the immune system. If this healthy microbiota is disrupted by antibiotics, chemotherapy, or a change in diet, intestinal colonization by pathogenic bacteria or viruses may occur, leading to disease. To manage substantial microbial exposure, epithelial surfaces of the intestinal tract produce a diverse arsenal of antimicrobial peptides (AMPs), including, of considerable importance, the β-defensins, which directly kill or inhibit the growth of microorganisms. Based on the literature data, the purpose of this work was to create a line of intestinal epithelial cells able to stably express gene encoding human β-defensin-2 (hBD-2) and human β-defensin-3 (hBD-3), in order to test their role in S. typhimurium infections and their interaction with the bacteria of the gut microbiota.