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Chlamydia  species infect a large range of vertebral hosts and have become of major economic and public health concern over the last decades. They are obligate intracellular bacteria that undergo a unique cycle of development characterized by the presence of two distinct bacterial forms. After infection of the host cell,  Chlamydia  are found inside a membrane-bound compartment, the inclusion. The surrounding membrane of the inclusion contributes to the host- Chlamydia  interface and specific pathogen-derived Inc proteins shape this interface allowing interactions with distinct cellular proteins. In contrast to many other bacteria,  Chlamydia  species acquire sphingomyelin from the host cell. In recent years a clearer picture of how  Chlamydia trachomatis  acquires this lipid emerged showing that the bacteria interact with vesicular and non-vesicular transport pathways that involve the recruitment of specific RAB proteins and the lipid-transfer protein CERT. These interactions contribute to the development of a new sphingomyelin-producing compartment inside the host cell. Interestingly, recruitment of CERT is conserved among different  Chlamydia  species including  Chlamydia psittaci . Here we discuss our current understanding on the molecular mechanisms used by  C. trachomatis  and  C. psittaci  to establish these interactions and to create a novel sphingomyelin-producing compartment inside the host cell important for the infection.

Sphingolipid Metabolism and Transport in Chlamydia trachomatis and Chlamydia psittaci Infections