Immunomodulation of macrophages by pathogenic Yersinia species

• Authors: K. Ruckdeschel
• Languages of publication: EN

Abstracts

EN

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 spp. engage a type III protein secretion system that mediates polarized translocation of Yersinia virulence factors, the so-called Yops, 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 the macrophage TNF- production and to macrophage apoptosis. The impairment of cellular functions results in a scenario, by which Yersinia efficiently resist 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.

Keywords

EN

APOPTOSIS; IMMUNOMODULATION; MACROPHAGE; YERSINIA

Discipline

• IMMUNOLOGY: IMMUNOLOGY

• Publisher: Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences
• Journal: Archivum Immunologiae et Therapiae Experimentalis
• Year: 2002
• Volume: 50
• Issue: 2
• Pages: 131-138

Contributors

author

K. Ruckdeschel

• Document Type: SHORT COMMUNICA
• Publication order reference: K.Ruckdeschel, Max von Pettenkofer-Institute for Hygiene and Medical Microbiology Pettenkoferstr. 9a, 80336 Munich, Germany