Bacterial responses to neutrophil phagocytosis.
OBJECTIVE
This review focuses on adaptive bacterial interactions with neutrophils, emphasizing information communicated within the past year about bacterial factors that respond to contact with or phagocytosis by PMN.


RESULTS
Since the discovery of type III and IV secretion, progress in the analysis of bacterial interactions with host phagocytes has been extensive but largely focused on the macrophage. The remarkable growth of information about bacterial subversion of macrophage metabolism has been summarized in several excellent reviews. The scope of progress on neutrophil-bacteria interactions is more limited and dominated by recent studies of the granulocyte pathogen, Anaplasma phagocytophilum, the agent of granulocytic ehrlichiosis.


CONCLUSIONS
For many pathogens, contact with or ingestion by phagocytes elicits a vigorous but varied microbial response. The response repertoire includes activation of type III and type IV secretion systems that inject effector molecules into the host cell. Effectors modify host cell signaling and metabolic pathways to favor survival of the microbe. Whereas microbial secretory structures are few in kind and relatively conserved, effector molecules are numerous and variable. Effectors may promote phagocytosis by nonphagocytic cells or suppress phagocytosis by macrophages and neutrophils. They may suppress assembly or misdirect localization of the phagocyte NADPH oxidase that is responsible for generating toxic oxidants, and they may suppress phagosome-lysosome fusion. Phagocytosed bacteria may also up-regulate the expression of defensive proteins that attenuate the effects of phagocyte-derived antimicrobial toxins. These pathogenic stratagems probably have their origins in the competition among single-celled organisms, eukaryotes versus prokaryotes, that arose early in evolution.
Rosen
Henry
H
Department of Medicine, University of Washington, Seattle 98195, USA. hqr@u.washington.edu
D041081:Anaplasma phagocytophilum / Q000472:pathogenicity; D000818:Animals; D001419:Bacteria / Q000472:pathogenicity*; D018407:Bacterial Physiological Phenomena; D004926:Escherichia coli / Q000472:pathogenicity; D009504:Neutrophils / Q000276:immunology / Q000382:microbiology*; D010587:Phagocytosis; D011550:Pseudomonas aeruginosa / Q000472:pathogenicity; D012486:Salmonella typhimurium / Q000472:pathogenicity; D015398:Signal Transduction; D013297:Streptococcus pyogenes / Q000472:pathogenicity; D015007:Yersinia / Q000472:pathogenicity