Fig 12.

Schematic of how stress-induced extracellular Hsp72 (eHsp72) could be a functionally significant danger signal to the immune system. Acute stress increases eHsp72 that accumulates at the site of inflammation and facilitates bacterial-stimulated NO and cytokines released by macrophages or neutrophils (or both). Potentiated NO and proinflammatory cytokines facilitate bacterial killing, resulting in faster inflammation resolution and improved host defense