Figure 6.

Schematic illustration of the interaction of acute and chronic inflammatory responses. (A) Induction of chronic partial ischaemia induces rapid recruitment of neutrophils and Gr1^high monocytes from the circulation. (B) Seven days after the induction of ischaemia, the neutrophilic inflammation has resolved, but an elevated population of Gr1^low MDCs persist in the tissue. (C) These Gr1^low MDCs are highly sensitive to a range of pharmacological or physiological stimuli (e.g. LPS or IR), and respond by generating a range of additional proinflammatory stimuli. (D) These secondary signals act on the endothelium to upregulate ICAM‐1 expression, which supports luminal neutrophil adhesion, and/or directly activate neutrophil chemotaxis. Naive tissues exposed to the same exogenous stimuli lack this additional source of secondary mediators, resulting in lower overall tissue activation.