Open AccessComparative Study of the Roles of AhpC and KatE as Respiratory Antioxidants inBrucella abortus2308
Author(s) -
Kendra H. Steele,
John E. Baumgartner,
Michelle Wright Valderas,
R. Martin Roop
Publication year - 2010
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.00231-10
Subject(s) - biology , catalase , virulence , mutant , peroxiredoxin , microbiology and biotechnology , endogeny , brucella abortus , nadph oxidase , reactive oxygen species , enzyme , biochemistry , peroxidase , gene , virology , brucellosis
Brucella strains are exposed to potentially toxic levels of H2 O2 both as a consequence of their aerobic metabolism and through the respiratory burst of host phagocytes. To evaluate the relative contributions of the sole catalase KatE and the peroxiredoxin AhpC produced by these strains in defense against H2 O2 -mediated toxicity, isogenickatE ,ahpC , andkatE ahpC mutants were constructed and the phenotypic properties of these mutants compared with those of the virulent parental strainB. abortus 2308. The results of these studies indicate that AhpC is the primary detoxifier of endogenous H2 O2 generated by aerobic metabolism. KatE, on the other hand, plays a major role in scavenging exogenous and supraphysiologic levels of H2 O2 , although this enzyme can play a supporting role in the detoxification of H2 O2 of endogenous origin if AhpC is absent.B. abortus ahpC andkatE mutants exhibit wild-type virulence in C57BL/6 and BALB/c mice, but theB. abortus ahpC katE double mutant is extremely attenuated, and this attenuation is not relieved in derivatives of C57BL/6 mice that lack NADPH oxidase (cybb) or inducible nitric oxide synthase (Nos2) activity. These experimental findings indicate that the generation of endogenous H2 O2 represents a relevant environmental stress thatB. abortus 2308 must deal with during its residence in the host and that AhpC and KatE perform compensatory roles in detoxifying this metabolic H2 O2 .