Figure 8. IL-1α acts as a factor to increase inflammation during infection and damage of cells.

Model showing that activation of TLRs following the binding of PAMPs, such as LPS from E. coli, stimulates accumulation of intracellular IL-1α (1), as well as secretion of other inflammatory mediators such as IL-6 (2). Subsequently, damage of cells releases IL-1α into the extracellular fluid (3), where it binds IL-1R1 on nearby cells to stimulate further secretion of IL-6 (4), and augment cellular inflammatory responses to pathogens when there is cell damage.