Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-5-22
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0004-069X
pubmed:author
pubmed:issnType
Print
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
131-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Immunomodulation of macrophages by pathogenic Yersinia species.
pubmed:affiliation
Max von Pettenkofer-Institute for Hygiene and Medical Microbiology, Munich, Germany. ruckdeschel@m3401.mpk.med.uni-muenchen.de
pubmed:publicationType
Journal Article, In Vitro, Review, Research Support, Non-U.S. Gov't