Emerging role of mitochondria in airborne particulate matter-induced immunotoxicity

Highlights: • Particulate matter (PM) targets the immune system and increases susceptibility to infections. • PM induces the derailment of mitochondrial machinery to modulate the immune response. • Upon damage, mtDNA escapes and triggers the TLR9, NLRP3 and cGAS-STING pathways. • Unraveling these mechanisms will help to identify biomarkers for PM linked immune disorders. The immune system is one of the primary targets of airborne particulate matter. Recent evidence suggests that mitochondria lie at the center of particulate matter-induced immunotoxicity. Particulate matter can directly interact with mitochondrial components (proteins, lipids, and nucleic acids) and impairs the vital mitochondrial processes including redox mechanisms, fusion-fission, autophagy, and metabolic pathways. These disturbances impede different mitochondrial functions including ATP production, which acts as an important platform to regulate immunity and inflammatory responses. Moreover, the mitochondrial DNA released into the cytosol or in the extracellular milieu acts as a danger-associated molecular pattern and triggers the signaling pathways, involving cGAS-STING, TLR9, and NLRP3. In the present review, we discuss the emerging role of mitochondria in airborne particulate matter-induced immunotoxicity and its myriad biological consequences in health and disease.