Open AccessThe impairment of methylmenaquinol:fumarate reductase affects hydrogen peroxide susceptibility and accumulation in C ampylobacter jejuni
Author(s) -
Kassem Issmat I.,
Khatri Mahesh,
Sanad Yasser M.,
Wolboldt Melinda,
Saif Yehia M.,
Olson Jonathan W.,
Rajashekara Gireesh
Publication year - 2014
Publication title -
microbiologyopen
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.881
H-Index - 36
ISSN - 2045-8827
DOI - 10.1002/mbo3.158
Subject(s) - fumarate reductase , catalase , hydrogen peroxide , chemistry , succinate dehydrogenase , intracellular , reductase , biochemistry , mutant , oxidative stress , campylobacter jejuni , wild type , microbiology and biotechnology , strain (injury) , periplasmic space , enzyme , bacteria , escherichia coli , biology , genetics , anatomy , gene
The methylmenaquinol:fumarate reductase (Mfr) of C ampylobacter jejuni is a periplasmic respiratory (redox) protein that contributes to the metabolism of fumarate and displays homology to succinate dehydrogenase (Sdh). Since chemically oxidized redox‐enzymes, including fumarate reductase and Sdh, contribute to the generation of oxidative stress in E scherichia coli , we assessed the role of Mfr in C . jejuni after exposure to hydrogen peroxide (H 2 O 2 ). Our results show that a Mfr mutant (∆ mfrA ) strain was less susceptible to H 2 O 2 as compared to the wildtype ( WT ). Furthermore, the H 2 O 2 concentration in the ∆ mfrA cultures was significantly higher than that of WT after exposure to the oxidant. In the presence of H 2 O 2 , catalase (KatA) activity and katA expression were significantly lower in the ∆ mfrA strain as compared to the WT . Exposure to H 2 O 2 resulted in a significant decrease in total intracellular iron in the ∆ mfrA strain as compared to WT , while the addition of iron to the growth medium mitigated H 2 O 2 susceptibility and accumulation in the mutant. The ∆ mfrA strain was significantly more persistent in RAW macrophages as compared to the WT . Scanning electron microscopy showed that infection with the ∆ mfrA strain caused prolonged changes to the macrophages’ morphology, mainly resulting in spherical‐shaped cells replete with budding structures and craters. Collectively, our results suggest a role for Mfr in maintaining iron homeostasis in H 2 O 2 stressed C . jejuni , probably via affecting the concentrations of intracellular iron.