Chlamydia and mitochondria - an unfragmented relationship.

Presence of pathogens within a eukaryotic cell is apt to generate stress. Such stress eventually leads to host defense responses, which includes, but is not limited to, apoptosis induction and subsequent destruction of the host cell and the pathogen. Obligate intracellular pathogens such as Chlamydia trachomatis are dependent on the survival of the host cell owing to their unique replication niche within a membrane-bound inclusion. Furthermore, being energy parasites, chlamydial development is strictly dependent on the host metabolism. Over the past decade the role of the small non-coding RNAs called microRNAs (miRNAs) have come into focus with respect to the regulation of apoptotic signaling, metabolic homeostasis and bacterial pathogenesis. Effect of Chlamydia infection on the host miRNA profile was hitherto unknown. In our recent work we demonstrated that Chlamydia infection induces and requires an upregulation of the host miRNA, miR-30c-5p (miR-30c) to ameliorate infection induced stress on the host mitochondrial architecture and hinders induction of apoptosis.