Abstract

Chlamydia trachomatis serovars are obligate intracellular bacterial pathogens mainly causing ocular and urogenital infections that affect millions of people worldwide and which can lead to blindness or sterility. They reside and multiply intracellularly within a membrane-bound vacuolar compartment, known as inclusion, and are characterized by a developmental cycle involving two morphologically and physiologically distinct chlamydial forms. Completion of the developmental cycle involves the secretion of > 70 C. trachomatis proteins that function in the host cell cytoplasm and nucleus, in the inclusion membrane and lumen, and in the extracellular milieu. These proteins can, for example, interfere with the host cell cytoskeleton, vesicular and non-vesicular transport, metabolism, and immune signalling. Generally, this promotes C. trachomatis invasion into, and escape from, host cells, the acquisition of nutrients by the chlamydiae, and evasion of cell-autonomous, humoral and cellular innate immunity. Here, we present an in-depth review on the current knowledge and outstanding questions about these C. trachomatis secreted proteins.

Highlights

  • Chlamydia trachomatis serovars are human pathogens causing mostly ocular and genital infections [1, 2]

  • There is functional evidence for secretion and effector role of CT166 (Chlamydia cytotoxin targeting Rac family small GTPase 1 (RAC1) that might contribute for downmodulating actin cytoskeleton changes during chlamydial invasion of host cells [197, 199]), CT619/CTL0883 and CT712/CTL0081, and CT847/CTL0217 in the host cell cytoplasm, and of GlgB, GlgP, MalQ and MrsA in the inclusion lumen [14, 289]

  • C. trachomatis has been shown to deliver at least ~60 proteins into the inclusion membrane and cytoplasm of host cells that function as effectors (Tables 1 and 2)

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Summary

Introduction

Chlamydia trachomatis serovars are human pathogens causing mostly ocular and genital infections [1, 2]. Several C. trachomatis Incs (MrcA (myosin regulatory complex subunit A), CT222, IPAM, CT224, CT228, IncB, IncC, CT288, and CT850; Table 1) have been shown to concentrate at regions of the inclusion membrane near the centrosome, known as inclusion microdomains, which are enriched in cholesterol and in the phosphorylated active form of Src family kinases [128].

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