Modulation of host mitochondrial dynamics during bacterial infection

Mitochondria is a dynamic organelle of the cell that can regulate and maintain cellular ATP level, ROS production, calcium signaling and immune response. In order to retain their shape and distribution, mitochondria go through coordinated cycles of fission and fusion. Further, dysfunctional mitochondria are selectively eliminated from the cell via mitophagy to synchronize mitochondrial quality control and cellular homeostasis. In addition, mitochondria when in close proximity with the endoplasmic reticulum can alter the signaling pathways and some recent findings also reveal a direct correlation between the mitochondrial localization in the cell to the immune response elicited against the invading pathogen. These modulations in the mitochondrial network are collectively termed as ‘mitochondrial dynamics’. Diverse bacteria, virus and parasitic pathogens upon infecting a cell can alter the host mitochondrial dynamics in favor of their multiplication and this in turn can be a major determinant of the disease outcome. Pharmacological perturbations in these pathways thus could lead to generation of additional therapeutic opportunities. This review will focus on the pathogenic modulation of the host mitochondrial dynamics, specifically during the bacterial infections and describes how dysregulated mitochondrial dynamics facilitates the pathogen's ability to establish efficient infection.