Título:	In vitro adhesion and invasion inhibition of Shigella dysenteriae, Shigella flexneri and Shigella sonnei clinical strains by human milk proteins
Autor(es):	Willer, Emerson da Motta Lima, Renato de Lourenço Giugliano, Loreny Gimenes
Assunto:	Cólon (Anatomia) - doenças Mortalidade Crianças Amamentação
Data de publicação:	28-Abr-2014
Editora:	BMC Microbiology
Referência:	WILLER, Emerson da Motta et al. In vitro adhesion and invasion inhibition of Shigella dysenteriae, Shigella flexneri and Shigella sonnei clinical strains by human milk proteins. BMC Microbiology, v. 4, Article 18, 28 abr. 2014. Disponível em: <https://bmcmicrobiol.biomedcentral.com/articles/10.1186/1471-2180-4-18>. Acesso em: 13 jun. 2017. doi: https://bmcmicrobiol.biomedcentral.com/articles/10.1186/1471-2180-4-18.
Abstract:	Background: Shigella is the etiological agent of shigellosis, a disease responsible for more than 500,000 deaths of children per year, in developing countries. These pathogens colonize the intestinal colon, invade, spreading to the other enterocytes. Breastfeeding plays a very important role in protecting infants from intestinal infections. Amongst milk compounds, glycosylated proteins prevent the adhesion of many enteropathogens in vitro. The aim of this work was to determine the effect of human milk proteins on the colonization potential of Shigella dysenteriae, S. flexneri and S. sonnei. To fulfill this purpose, pooled milk samples from five donors, were fractionated by gel filtration and affinity chromatography. Using tissue culture, the milk fractions obtained were tested in Shigella adhesion and invasion assays. Results: Our revealed showed that both adhesion and invasion of Shigella species were inhibited by low concentration of secretory immunoglobulin A, lactoferrin and free secretory component. This work also showed that, these proteins bind to superficial and whole-cell Shigella proteins. Conclusions: Our findings suggest that human milk may act inhibiting adhesion and, consequently, invasion of Shigella, thereafter preventing shigellosis in infants.
Licença:	© 2004 Willer et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
DOI:	https://dx.doi.org/10.1186/1471-2180-4-18
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