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Cytotoxic necrotizing factor type 1 production by uropathogenic Escherichia coli modulates polymorphonuclear
Jon M Davis1, Susan B Rasmussen, Alison D O'Brien
1Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, B4052, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, USA.
Infection and Immunity
|August 23, 2005
Summary
Cytotoxic necrotizing factor type 1 (CNF1) produced by uropathogenic Escherichia coli (UPEC) helps bacteria survive. CNF1 impairs mouse polymorphonuclear leukocytes (PMNs) by altering their function, aiding UPEC evasion.
Area of Science:
- Microbiology
- Immunology
- Molecular Biology
Background:
- Uropathogenic Escherichia coli (UPEC) utilizes virulence factors like cytotoxic necrotizing factor type 1 (CNF1) to cause infection.
- CNF1 activates Rho GTPases, influencing host cell functions and contributing to UPEC virulence in urinary tract infections and prostatitis.
- Previous studies noted elevated polymorphonuclear leukocytes (PMNs) in CNF1-positive UPEC infections and prolonged bacterial survival with human neutrophils.
Purpose of the Study:
- To investigate if CNF1 production by UPEC diminishes the antimicrobial capacity of mouse PMNs.
- To determine if CNF1 affects phagocyte function by targeting Rho family GTPases critical for phagocytosis and reactive oxygen species generation.
Main Methods:
- Incubation of UPEC strains (CNF1-positive and negative) with mouse PMNs.
- Assessment of bacterial survival within PMNs.
- Analysis of PMN phagocytosis, complement receptor CR3 distribution, intracellular respiratory burst, and Rac2 activation.
Main Results:
- CNF1 synthesis conferred a survival advantage to UPEC incubated with mouse PMNs, similar to observations with human neutrophils.
- CNF1-positive UPEC down-regulated phagocytosis by PMNs.
- CNF1-positive UPEC altered CR3 distribution, enhanced intracellular respiratory burst, and increased Rac2 activation in PMNs.
Conclusions:
- CNF1 production by UPEC modulates mouse PMN function, facilitating bacterial survival during the acute inflammatory response.
- Targeting Rho family GTPases by CNF1 is a key mechanism for UPEC to evade innate immune defenses mediated by PMNs.