Essential role of YopD in inhibition of the respiratory burst of macrophages by Yersinia enterocolitica.

摘要: The respiratory burst is a key element of the bactericidal armamentarium phagocytes. In this study we have shown that virulent strain Yersinia enterocolitica serogroup O:9 completely inhibited ability murine bone marrow-derived macrophages to mount in response stimulation by zymosan. This property bacterium was abrogated curing its 71.5-kb virulence plasmid and transposon mutagenesis plasmid-borne yopD gene. Derivatives which were unable inhibit also less able disrupt cytoskeletal actin resist phagocytosis. mutants showed an impaired dephosphorylate phosphotyrosine residues macrophage proteins avirulent for mice. All these defects fully or partly restored trans-complementation mutant with cloned results those previous work YopD (R. Rosqvist, A. Forsberg, H. Wolf-Watz, Infect. Immun. 59:4562-4569, 1991) suggest functions chiefly facilitating transport plasmid-encoded proteins, such as YopE, cytotoxin, YopH, protein tyrosine phosphatase, across cytoplasmic membrane their targets within host cells. combined action Yops on especially actin, could explain effects Y. morphology, phagocytic capacity, activity, all rely integrity function normally.