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. Author manuscript; available in PMC: 2020 Jan 29.
Published in final edited form as: Curr Transplant Rep. 2019 Jan 29;6(1):78–89. doi: 10.1007/s40472-019-0230-4

Figure 1. Putative mechanisms of neutrophil recruitment in liver ischemia-reperfusion injury.

Figure 1.

(A) Liver-resident Kupffer cells and liver sinusoidal endothelial cells (LSECs) sense initial danger-associated molecular patterns (DAMPs) via pattern recognition receptors (PRRs) to trigger intercellular adhesion molecule-1 (ICAM-1) expression on endothelial cells and neutrophil adhesion by integrin αMβ2 (Mac-1) signaling. (B) Neutrophils move on the LSECs luminal side toward the damaged site, guided by Kupffer cell-derived chemokine (CXCL1/CXCL2) gradient. (C) Neutrophils detect mitochondrial N-formyl peptides (FMIT) via formyl peptide receptor 1 (FPR1) and migrate underneath LSECs toward the injury site. (D) Neutrophils express and secret matrix metalloproteinase 9 (MMP9) to degrade extracellular matrix (ECM) during migration.