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Protection of epithelial cells from Salmonella enterica serovar Enteritidis invasion by antibodies against the SPI-1 type III secretion system

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Abstract:

Salmonella enterica serovar Enteritidis (Salmonella Enteritidis) is one of the major causes of bacterial food-borne illness in humans. During the course of infection, Salmonella Enteritidis uses 2 type III secretion systems (T3SS), one of which is encoded on Salmonella pathogenicity island 1 (SPI-1). SPI-1 plays a major role in the invasion process. In the present study, we evaluated the effect of sera against the SPI-1 T3SS components on invasion in vitro using polarized human intestinal epithelial cells (Caco-2). Antisera to SipD protected Caco-2 cells against entry of wild-type Salmonella Enteritidis. On the other hand, sera against InvG, PrgI, SipA, SipC, SopB, SopE, and SopE2 did not affect Salmonella Enteritidis entry. To illustrate the specificity of anti-SipD mediated inhibition, SipD-specific antibodies were depleted from the serum. Antiserum depleted of SipD-specific antibodies lost its capacity to inhibit Salmonella Enteritidis entry. Thus, we demonstrate for the first time that antibodies against the SPI-1 needle tip protein (SipD) inhibit Salmonella Enteritidis invasion and that the SipD protein may be an important target in blocking SPI-1 mediated virulence of Salmonella Enteritidis.

Salmonella enterica sérotype Enteritidis (Salmonella Enteritidis) est une des causes principales des maladies bactériennes transmissibles d’origine alimentaire chez l’humain. Au cours du processus d’infection, Salmonella Enteritidis utilise un système de sécrétion de type III (T3SS), dont l’un est codé sur l’îlot de pathogénicité chromosomique SPI-1 (Salmonella pathogenicity island 1). SPI-1 joue un rôle majeur dans le processus d’invasion. Dans cette étude, nous avons évalué l’effet d’un antisérum dirigé contre les composantes du SPI-1 de T3SS sur l’invasion in vitro de cellules intestinales épithéliales polarisées humaines (Caco-2). Un antisérum dirigé contre SipD a protégé les cellules Caco-2 contre l’entrée de Salmonella Enteritidis sauvage. Au contraire, des antisérums dirigés contre InvG, PrgI, SipA, SipC, SopB, SopE et SopE2 n’ont pas affecté l’entrée de Salmonella Enteritidis. Afin d’illustrer la spécificité de l’inhibition dépendante de l’anti-SipD, les anticorps spécifiques à SipD ont été retirés du sérum. L’antisérum dépourvu d’anticorps spécifiques à SipD avait perdu sa capacité d’inhiber l’entrée de Salmonella Enteritidis. Ainsi, nous démontrons pour la première fois que des anticorps dirigés contre la protéine en forme d’aiguille SipD inhibent l’invasion par Salmonella Enteritidis et que SipD peut être une cible importante pour bloquer la virulence dépendante de SPI-1 de Salmonella Enteritidis.

Document Type: Research Article

Publication date: June 1, 2010

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  • Published since 1954, this monthly journal contains new research in the field of microbiology including applied microbiology and biotechnology; microbial structure and function; fungi and other eucaryotic protists; infection and immunity; microbial ecology; physiology, metabolism and enzymology; and virology, genetics, and molecular biology. It also publishes review articles and notes on an occasional basis, contributed by recognized scientists worldwide.
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