Abstract
The EnvZ/OmpR two-component system constitutes a regulatory pathway involved in bacterial adaptive responses to environmental cues. Our previous findings indicated that the OmpR regulator in Yersinia enterocolitica O:9 positively regulates the expression of FlhDC, the master flagellar activator, which influences adhesion/invasion properties and biofilm formation. Here we show that a strain lacking OmpR grown at 37°C exhibits extremely high resistance to the bactericidal activity of normal human serum (NHS) compared with the wild-type strain. Analysis of OMP expression in the ompR mutant revealed that OmpR reciprocally regulates Ail and OmpX, two homologous OMPs of Y. enterocolitica, without causing significant changes in the level of YadA, the major serum resistance factor. Analysis of mutants in individual genes belonging to the OmpR regulon (ail, ompX, ompC and flhDC) and strains lacking plasmid pYV, expressing YadA, demonstrated the contribution of the respective proteins to serum resistance. We show that Ail and OmpC act in an opposite way to the OmpX protein to confer serum resistance to the wild-type strain, but are not responsible for the high resistance of the ompR mutant. The serum resistance phenotype of ompR seems to be multifactorial and mainly attributable to alterations that potentiate the function of YadA. Our results indicate that a decreased level of FlhDC in the ompR mutant cells is partly responsible for the serum resistance and this effect can be suppressed by overexpression of flhDC in trans. The observation that the loss of FlhDC enhances the survival of wild-type cells in NHS supports the involvement of FlhDC regulator in this phenotype. In addition, the ompR mutant exhibited a lower level of LPS, but this was not correlated with changes in the level of FlhDC. We propose that OmpR might alter the susceptibility of Y. enterocolitica O:9 to complement-mediated killing through remodeling of the outer membrane.
Highlights
The human enteropathogen Yersinia enterocolitica is the causative agent of yersiniosis: an acute or chronic zoonotic disease producing a variety of clinical symptoms, i.e. intestinal, pseudoappendicular, erythematous and septicaemic [1]
Using an ompR mutant (DompR::Km) of Y. enterocolitica Ye9 constructed by a reverse genetics polymerase chain reaction (PCR)-based strategy, we previously showed that OmpR is involved in the response of this bacterium to environmental stresses, and reciprocally regulates invasion and motility, which may confer an advantage in particular ecological niches [15,17,18,19]
Another important property of enteropathogens is their ability to resist the bactericidal effects of normal human serum (NHS) and experiments were performed to determine whether OmpR can influence the susceptibility of Y. enterocolitica Ye9 to complement-dependent killing
Summary
The human enteropathogen Yersinia enterocolitica is the causative agent of yersiniosis: an acute or chronic zoonotic disease producing a variety of clinical symptoms, i.e. intestinal, pseudoappendicular, erythematous and septicaemic [1]. After Campylobacter jejuni and Salmonella spp., Y. enterocolitica is the third most common enteric pathogen associated with foodborne infections in Europe [2]. Before Y. enterocolitica infects a mammalian host the bacteria must survive free-living in the environment. Yersiniae cells have to adapt to the host body temperature (37uC), and survive in the face of various unfavorable environmental factors and the immune system. Switching between distinct niches within and outside the host presents Y. enterocolitica with a constant adaptive challenge. In response to different environmental cues, the pathogenic Y. enterocolitica synthesizes several chromosomal- and plasmid (pYV)-encoded virulence factors whose expression is tightly regulated [3,4]
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