Plasmid-mediated resistance to phagocytosis in Yersinia enterocolitica

Abstract

Results of our previous studies have shown that the chemiluminescence response of human neutrophils (polymorphonuclear leukocytes [PMNs]) is inhibited by plasmid-mediated cell surface components from Yersinia enterocolitica. In this study we examined the susceptibility to phagocytosis of Y. enterocolitica cells with or without plasmid-mediated surface structure and the effect of isolated outer membrane fragments on phagocytosis of Escherichia coli by PMNs in vitro. Y. enterocolitica cells with expressed plasmid-mediated surface structure were much less sensitive to ingestion by PMNs than those without it, and the resistance to phagocytosis was readily eliminated in a dose-dependent fashion by pronase treatment of whole cells, which was shown to remove plasmid-encoded outer membrane proteins. Ingestion and intracellular killing of E. coli were inhibited significantly in the presence of isolated outer membrane fragments derived from plasmid-bearing Y. enterocolitica cells. To assess the interaction of Y. enterocolitica with phagocytic cells in vivo, two isogenic strains of Y. enterocolitica, differing only in the presence or absence of the virulence plasmid, were inoculated intradermally into the backs of rabbits; and tissue sections obtained at 12 h postinoculation were examined by light and electron microscopy. The plasmidless strain was found almost entirely in PMNs or mononuclear cells. In contrast, the plasmid-bearing strain was found to be surrounded by, or interspersed with, PMNs and mononuclear cells; but most bacteria were extracellular, with little evidence of phagocytosis. These results suggest that plasmid-mediated cell surface components of Y. enterocolitica act as antiphagocytic factors, thus facilitating the survival and proliferation of the organism in the host tissue.

Yersiniaprotein kinase A phosphorylates vasodilator-stimulated phosphoprotein to modify the host cytoskeleton

“…Yersinia enterocolitica and Y. pseudotuberculosis are human enteropathogenic species that cause self-limited gastrointestinal disorders, while Y. pestis caused deadly plague that has been responsible for three pandemics in human history, including the notorious Black Death (Prentice and Rahalison, 2007;Haensch et al, 2010). Pathogenic Yersinia needs to escape from the professional phagocytes to establish successful infection (Lian et al, 1987). Many virulence factors contribute to its antiphagocytic ability, including the well-known type III secretion system (T3SS) encoded by a 70 kb pCD1/pYV plasmid, which is shared by Y. pestis and the enteropathogenic Yersiniae (Viboud and Bliska, 2005).…”

The InhA1 metalloprotease allows spores of the B. cereus group to escape macrophages

“…Several bacterial pathogens have evolved strategies to survive the attack by professional phagocytes. Yersinia enterocolitica and Helicobacter pylori block phagocytosis by monocytes and neutrophils, allowing the pathogen to survive on the cell surface (Lian et al ., 1987;Ramarao et al ., 2000;Ramarao and Meyer, 2001). Shigella and Listeria escape into the cytoplasm where they replicate (Sansonetti et al ., 1986;Cossart and Lecuit, 1998).…”

Chromosome-mediated resistance of Yersinia enterocolitica serotype O9 to intracellular killing by mouse peritoneal macrophages

“…The ail locus is related to the invasive phenotype, and it has been uniquely mechanisms. It has been reported that plasmidencoded proteins protect bacteria from phagocytosis and destruction by professional phagocytes [7][8][9][10]. Some of these experiments were done as indirect measures of phagocytic activity by chemiluminescence assays, or by use of Escherichia coli as a probe organism [8,9].…”

“…It has been reported that plasmidencoded proteins protect bacteria from phagocytosis and destruction by professional phagocytes [7][8][9][10]. Some of these experiments were done as indirect measures of phagocytic activity by chemiluminescence assays, or by use of Escherichia coli as a probe organism [8,9]. Recently, the mouse model of yersiniosis has been used to study the innate immune mechanisms against infection with Y. enterocolitica serotype 08, and the importance of the plasmid-mediated resistance to in vivo phagocytosis has been established [7].…”