Abstract
Francisella tularensis is a Gram-negative, facultative intracellular pathogen and the causative agent of a lethal human disease known as tularemia. Due to its extremely high virulence and potential to be used as a bioterror agent, F. tularensis is classified by the CDC as a Category A Select Agent. As an intracellular pathogen, F. tularensis during its intracellular residence encounters a number of oxidative and nitrosative stresses. The roles of the primary antioxidant enzymes SodB, SodC and KatG in oxidative stress resistance and virulence of F. tularensis live vaccine strain (LVS) have been characterized in previous studies. However, very fragmentary information is available regarding the role of peroxiredoxin of the AhpC/TSA family (annotated as AhpC) of F. tularensis SchuS4; whereas the role of AhpC of F. tularensis LVS in tularemia pathogenesis is not known. This study was undertaken to exhaustively investigate the role of AhpC in oxidative stress resistance of F. tularensis LVS and SchuS4. We report that AhpC of F. tularensis LVS confers resistance against a wide range of reactive oxygen and nitrogen species, and serves as a virulence factor. In highly virulent F. tularensis SchuS4 strain, AhpC serves as a key antioxidant enzyme and contributes to its robust oxidative and nitrosative stress resistance, and intramacrophage survival. We also demonstrate that there is functional redundancy among primary antioxidant enzymes AhpC, SodC, and KatG of F. tularensis SchuS4. Collectively, this study highlights the differences in antioxidant defense mechanisms of F. tularensis LVS and SchuS4.
Highlights
Francisella tularensis is a Gram-negative, facultative intracellular pathogen and the causative agent of a lethal human disease known as tularemia
It was observed that growth pattern of the ΔahpC mutant was identical to that of the wild type F. tularensis live vaccine strain (LVS) or the transcomplemented strain when grown aerobically indicating that the loss of alkyl hydroperoxide reductase (ahpC) is not associated with any growth defect in the ΔahpC mutant (Fig 1B)
Very fragmentary information is available regarding the role of both SodC and AhpC [16] of F. tularensis SchuS4, and none related to AhpC of F. tularensis LVS
Summary
Francisella tularensis is a Gram-negative, facultative intracellular pathogen and the causative agent of a lethal human disease known as tularemia. F. tularensis has a very broad host range and can infect a wide range of ticks, arthropods, and mammals [1]. Tularensis (Type A) cause lethal tularemia in North America. The strains belonging to F. tularensis subsp. Holarctica (Type B) are less infectious than the Type A strains and are prevalent. Oxidative stress resistance mechanisms of Francisella tularensis exist regarding the contents of the manuscript and its authors The strains belonging to F. tularensis subsp. holarctica (Type B) are less infectious than the Type A strains and are prevalent
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