Mitochondria affect antibacterial immunity in cross talk with innate immune response molecules coded by genes of nuclear origin.

Introduction: Mitochondria are dynamic, semi-autonomous organelles that, in addition to their central role in ATP production, regulate calcium homeostasis, iron metabolism, apoptosis, and innate immune signalling. Although the mitochondrial genome encodes only 37 genes, mitochondrial architecture, bioenergetic function, and dynamics are governed predominantly by nuclear-encoded proteins, necessitating highly coordinated communication between mitochondrial DNA (mtDNA) and the nuclear genome. Disruption of this bidirectional mitochondrial-nuclear crosstalk has been increasingly implicated in the pathogenesis of numerous diseases across species; however, the molecular mechanisms underlying this communication remain incompletely understood. Materials and method: In the present study, we used Result and discussion: Our findings demonstrate that the mitochondrially encoded proteins cytochrome b and cytochrome c functionally interact with the nuclear-encoded immune regulators NLRP3, IL-18, and STING through the NOD-like receptor signalling pathway, phagocytic pathways, and the cytosolic DNA-sensing pathway. Furthermore, molecular docking analyses identified putative interaction sites between IL-18 and