Immunomodulation of macrophages by pathogenic Yersinia species.
The interaction between macrophages and bacterial pathogens plays a crucial role in the pathogenesis of infectious diseases. Pathogenic species of the Gram-negative bacterium Yersinia deploy complex strategies to disarm macrophages and to disrupt their response to infection. For this purpose, Yersinia sp. engage a type III protein secretion system that mediates the polarized translocation of Yersinia virulence factors, the so-called Yops (Yersinia outer proteins), into the host cell cytoplasm. There, the Yops act on different cellular levels to neutralize a sequence of programmed phagocyte effector functions. Yersiniae initially impair the phagocytic machinery and block the generation of the bactericidal oxidative burst. Furthermore, yersiniae uncouple an array of fine-tuned signals of innate immunity, which leads to suppression of macrophage TNF-alpha production and to macrophage apoptosis. The impairment of cellular functions results in a scenario by which Yersinia efficiently resists the attack of the macrophage and finally kills the macrophage by activating its intrinsic cell suicide mechanism. This review highlights the aspects of Yersinia-macrophage interaction that determine the fate of the infected cell.
Ruckdeschel
Klaus
K
Max von Pettenkofer-Institute for Hygiene and Medical Microbiology, Munich, Germany. ruckdeschel@m3401.mpk.med.uni-muenchen.de
D000818:Animals; D017209:Apoptosis; D001425:Bacterial Outer Membrane Proteins / Q000502:physiology; D006801:Humans; D066298:In Vitro Techniques; D008264:Macrophages / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology / Q000502:physiology; D008954:Models, Biological; D010587:Phagocytosis; D015398:Signal Transduction; D014774:Virulence / Q000276:immunology; D015007:Yersinia / Q000276:immunology / Q000472:pathogenicity*
D001425:Bacterial Outer Membrane Proteins