Resistance of Francisella tularensis strains against reactive nitrogen and oxygen species with special reference to the role of KatG

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TypeArticle
Journal titleAcoustics, Speech, and Signal Processing Newsletter, IEEE
Volume75
Issue3
Pages13031309; # of pages: 7
SubjectAnimals; bacterial; Bacterial Proteins; Catalase; cell; CELLS; Cells,Cultured; DIFFERENCE; Drug Resistance,Multiple,Bacterial; enzymology; Francisella tularensis; In Vitro; INHIBITOR; MECHANISMS; metabolism; Mice; Mice,Inbred C57BL; Microbiology; MUTANT; MUTANTS; Nitrogen; Oxygen; pathogenicity; physiology; RATES; Reactive Nitrogen Species; Reactive Oxygen Species; Role; STRAIN; STRAINS; SYSTEM; Virulence
AbstractFrancisella tularensis is a facultative intracellular bacterial pathogen capable of proliferating within host macrophages. The mechanisms that explain the differences in virulence between various strains of the species are not well characterized. In the present study, we show that both attenuated (strain LVS) and virulent (strains FSC200 and SCHU S4) strains of the pathogen replicate at similar rates in resting murine peritoneal exudate cells (PEC). However, when PEC were activated by exposure to gamma interferon (IFN-gamma), they killed LVS more rapidly than virulent strains of the pathogen. Addition of N(G)-monomethyl-l-arginine, an inhibitor of inducible nitric oxide synthase, to IFN-gamma-treated PEC, completely inhibited killing of the virulent strains, whereas it only partially blocked the killing of LVS. Similarly, in a cell-free system, SCHU S4 and FSC200 were more resistant to killing by H(2)O(2) and ONOO(-) than F. tularensis LVS. Catalase encoded by katG is a bacterial factor that can detoxify bactericidal compounds such as H(2)O(2) and ONOO(-). To investigate its contribution to the virulence of F. tularensis, katG deletion-containing mutants of SCHU S4 and LVS were generated. Both mutants demonstrated enhanced susceptibility to H(2)O(2) in vitro but replicated as effectively as the parental strains in unstimulated PEC. In mice, LVS-DeltakatG was significantly attenuated compared to LVS whereas SCHU S4-DeltakatG, despite slower replication, killed mice as quickly as SCHU S4. This implies that clinical strains of the pathogen have katG-independent mechanisms to combat the antimicrobial effects exerted by H(2)O(2) and ONOO(-), the loss of which could have contributed to the attenuation of LVS
Publication date
LanguageEnglish
AffiliationNational Research Council Canada; NRC Institute for Biological Sciences
Peer reviewedNo
NRC numberLINDGREN2007
NPARC number9387813
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Record identifier5cb9c3c6-479f-4fb8-adae-34b768f68d51
Record created2009-07-10
Record modified2016-05-09
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