MOTS-c, a mitochondrial-encoded microprotein, has immunological origins and functions, revealing for the first time that our immune system is encoded by both co-evolved nuclear and mitochondrial genomes.
In a mouse model of E. coli meningitis, non-myeloid TLR4 signaling is a key determinant of the inflammatory response in all leptomeningeal cells and of the increase in vascular permeability.
Inflammatory activation of endothelial cells triggers Pink1-dependent mitophagy and mitochondrial formyl peptides release, which drives neutrophil recruitment and lung injury.
