Abstract

Bacteria exposed to host serum are subject to the antibacterial effects to the complement system. However, pathogenic microorganisms have evolved mechanisms of evading this immune attack. We have previously demonstrated that at least two R. conorii antigens, RC1281/Adr1 and OmpB β-peptide, contribute to the evasion of complement-mediated killing by binding the complement regulatory proteins vitronectin and factor H. RC1282/Adr2, a protein related to Adr1, is predicted to share similar structural features, suggesting that this protein may also contribute to evasion of complement-mediated killing. Interestingly, the R. prowazekii Adr1 and Adr2(RP828) proteins were originally found to interact with host cell surface proteins, suggesting their putative roles as adhesins in this pathogenic rickettsial species. In this study, we expressed both R. conorii and R. prowazekii Adr2 on the surface of a non-adherent, serum-sensitive strain of E. coli to examine the potential role of this protein to mediate evasion of complement-mediated killing and adherence to host cells. We demonstrate that, similar to R. conorii Adr1, R. conorii and R. prowazekii Adr2 are sufficient to mediate serum resistance and to promote interaction with the host complement regulator vitronectin. Furthermore, we demonstrate that expression of Adr2 in a non-adherent strain of E. coli is insufficient to mediate adherence to cultured mammalian endothelial cells. Together, our data demonstrate that the R. conorii and R. prowazekii Adr2 protein does not participate in the interactions with mammalian cells, but rather, participates in the evasion of killing by complement.

Highlights

  • Rickettsia conorii is a small Gram-negative, obligate-intracellular bacterium, and the etiological agent of endemic Mediterranean spotted fever (MSF)

  • We have previously demonstrated that R. conorii remains viable in the presence of serum complement proteins, and that depletion of one of these regulatory proteins, such as factor H and vitronectin, is not sufficient to completely ablate serum sensitivity [10, 11]

  • Probing with an anti-vitronectin antibody revealed a reactive band at approximately 75 kDa in lysates of Adr2 expressing E. coli, but not in the lanes containing pAF17 lysate (Figs 4B and 5B). These results demonstrate that direct Vn binding by Adr2 is a phenotype conserved across both Spotted fever group (SFG) and Typhus Group (TG) rickettsial species

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Summary

Introduction

Rickettsia conorii is a small Gram-negative, obligate-intracellular bacterium, and the etiological agent of endemic Mediterranean spotted fever (MSF). MSF is transmitted by an arthropod vector, and subsequent dissemination of the microbe throughout a human host results in the development of a characteristic maculopapular dermal rash [1].

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