The impairment of methylmenaquinol:fumarate reductase affects hydrogen peroxide susceptibility and accumulation in Campylobacter jejuni
Version of Record online: 7 FEB 2014
© 2014 The Authors. MicrobiologyOpen published by John Wiley & Sons Ltd.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Volume 3, Issue 2, pages 168–181, April 2014
How to Cite
MicrobiologyOpen 2014; 3(2): 168–181
- Issue online: 9 APR 2014
- Version of Record online: 7 FEB 2014
- Manuscript Accepted: 26 DEC 2013
- Manuscript Revised: 7 DEC 2013
- Manuscript Received: 16 AUG 2013
- Ohio Agricultural Research and Development Center
- Ohio State University
- C. jejuni ;
- hydrogen peroxide resistance;
- methylmenaquinol:fumarate reductase;
The methylmenaquinol:fumarate reductase (Mfr) of Campylobacter 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 Escherichia coli, we assessed the role of Mfr in C. jejuni after exposure to hydrogen peroxide (H2O2). Our results show that a Mfr mutant (∆mfrA) strain was less susceptible to H2O2 as compared to the wildtype (WT). Furthermore, the H2O2 concentration in the ∆mfrA cultures was significantly higher than that of WT after exposure to the oxidant. In the presence of H2O2, catalase (KatA) activity and katA expression were significantly lower in the ∆mfrA strain as compared to the WT. Exposure to H2O2 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 H2O2 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 H2O2 stressed C. jejuni, probably via affecting the concentrations of intracellular iron.