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Sensing Mg 2+ contributes to the resistance of Pseudomonas aeruginosa to complement‐mediated opsonophagocytosis
Author(s) -
Qadi Mohammad,
IzquierdoRabassa Sofía,
Mateu Borrás Margalida,
DoménechSánchez Antonio,
Juan Carlos,
Goldberg Joanna B.,
Hancock Robert E. W.,
Albertí Sebastián
Publication year - 2017
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.13889
Subject(s) - pseudomonas aeruginosa , virulence , microbiology and biotechnology , biology , mutant , bacterial outer membrane , western blot , bacteria , two component regulatory system , complement system , gene , biochemistry , genetics , escherichia coli , antibody
Summary Pseudomonas aeruginosa adaptation to survive in the host hinges on its ability to probe the environment and respond appropriately. Rapid adaptation is often mediated by two‐component regulatory systems, such as the PhoP/PhoQ system that responds to Mg 2+ ion concentration. However, there is limited information about the role of PhoQ in P. aeruginosa bloodstream infections. We used a murine model of systemic infection to test the virulence of a PhoQ‐deficient mutant. Mutation of PhoQ impaired the virulence and the ability to cause bacteremia of P. aeruginosa . In the presence of blood concentrations of Mg 2+ , a PhoQ mutant bound more C3 and was more susceptible to complement‐mediated opsonophagocytosis than the parent strain, suggesting a direct effect of the Mg 2+ on the modulation of expression of a bacterial component controlled by the PhoP/PhoQ system. Ligand blot analysis, C3 binding experiments and opsonophagocytosis assays identified this component as the outer membrane protein OprH, expression of which impaired the virulence of P. aeruginosa in a murine model of systemic infection. We demonstrate that expression of PhoQ is essential to detect Mg 2+ and reduce the expression of OprH, a previously unrecognized C3 binding molecule that promotes the opsonophagocytosis of P. aeruginosa .