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Abstract

Chlamydia is an intracellular bacterial pathogen responsible for a high burden of disease globally. In order to survive within the host cell, the pathogen hijacks the host to engineer an intracellular niche termed "inclusion". The inclusion provides a permissive environment and protects the pathogen from the innate immune system. Using molecular tools and live cell imaging, we have revealed several intracellular pathways that the pathogen utilizes in order to survive and replicate inside the host. Chlamydia trachomatis depends on its ability to acquire host-derived nutrients, in particular Golgi-derived lipids. Using chemical inhibitors, live-cell imaging and Rab6 knockdown cells, we have shown that stable microtubules, distinct networks of dynamic MTs, acquire unique posttranslational modifications upon Chlamydia infection of human epithelial cells, which are required for optimum growth. Through promoting the formation of long-lived, stabilized microtubules, in particular detyrosinated microtubules, Chlamydia ensures that Golgi stacks are remodelled to the surface of the inclusion. In addition, we have shown that acute chlamydial infection induces degradation of the tumour suppressor p53, which is mediated by Murine Double Minute 2 (MDM2), and is responsible for the apoptosis resistance of infected cells. Chlamydia thus modulates stress-related signalling pathways to maintain host cell viability and ensure completion of its life cycle. Furthermore, we have also shown that Chlamydia evades the innate immune response of the host by inhibiting nitric oxide production through induction of the alternative polyamine pathway.

Biography

Munir A Al-Zeer has completed his PhD and has published few articles in the reputed journals. He is currently doing his post-doctoral from Max Planck Institute in Germany.

Email: al-zeer@mpiib-berlin.mpg.de