Abstract
Dynamic interactions that govern the balance between host and pathogen determine the outcome of infection and are shaped by evolutionary pressures. Eukaryotic hosts have evolved elaborate and formidable defense mechanisms that provide the basis for innate and adaptive immunity. Proteins containing a membrane attack complex/Perforin (MACPF) domain represent an important class of immune effectors. These pore-forming proteins induce cell killing by targeting microbial or host membranes. Intracellular bacteria can be shielded from MACPF-mediated killing, and Chlamydia spp. represent a successful paradigm of obligate intracellular parasitism. Ancestors of present-day Chlamydia likely originated at evolutionary times that correlated with or preceded many host defense pathways. We discuss the current knowledge regarding how chlamydiae interact with the MACPF proteins Complement C9, Perforin-1, and Perforin-2. Current evidence indicates a degree of resistance by Chlamydia to MACPF effector mechanisms. In fact, chlamydiae have acquired and adapted their own MACPF-domain protein to facilitate infection.
Highlights
Obligate intracellular bacteria depend on survival within eukaryotic host cells
Given the apparent long co-evolution of the host-pathogen interaction exemplified by Chlamydia, this review will summarize current evidence of chlamydial resistance and susceptibility to membrane attack complex/Perforin (MACPF) domain-mediated attack strategies while highlighting immune evasion mechanisms adapted through co-evolution
In experiments using C3 deficient mice, C. muridarum infectivity was not impacted during genital infections [29], C. psittaci pneumonia was significantly exacerbated when chlamydiae were introduced via a respiratory route [30]. These data raise the possibility that C5b-C8 recruitment of C9 and pore formation may lead to fatal disruption of the chlamydial envelope; yet, formation of the membrane attack complex (MAC) appears to be dispensable as a primary control mechanism for Chlamydia infections
Summary
Obligate intracellular bacteria depend on survival within eukaryotic host cells. The family Chlamydiaceae contains at least nine designated species of obligate intracellular pathogens exhibiting a diverse host range in higher eukaryotes. Formation of targeted membrane spanning pores using membrane attack complex/Perforin (MACPF)-domain proteins represents one mechanism used by both innate and adaptive arms of immunity.
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