1. Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2017.183
Figure 2 Kupffer cells and neutrophils cooperate to capture bacteria in the liver vasculature
Figure 2 | Kupffer cells and neutrophils cooperate to capture bacteria in the liver vasculature. Kupffer cells capture circulating pathogens in the liver sinusoids. Complement receptor of immunoglobulin superfamily (CRIg) functions as a pattern recognition receptor on Kupffer cells to directly bind Gram-positive bacteria such as Staphylococcus aureus via lipoteichoic acid (LTA) recognition. CRIg also functions as a complement receptor. Neutrophils lack CRIg and contribute to bacterial catching and killing by neutrophil extracellular trap (NET) formation. Chemokines produced by Kupffer cells, as well as the activation of endothelial Toll-like receptor 4 (TLR4), coordinate neutrophil adhesion and recruitment to the liver. Activated endothelial cells induce the deposition of serum-derived hyaluronan-associated protein (SHAP; also known as ITIH1) within sinusoids, which is required for CD44-dependent and hyaluronan-dependent neutrophil adhesion. The aggregation of platelets by platelet glycoprotein Ib (GPIB)–von Willebrand factor (vWF) binding to Kupffer cells facilitates bacterial clearance. TLR4-dependent platelet–neutrophil interaction increases NET formation. NETs contain antimicrobial molecules, such as histones and elastases, which contribute to bacterial killing. NETs are anchored by the interaction between histones and endothelial vWF. E. coli, Escherichia coli; LFA1, lymphocyte function-associated antigen 1.
Honda, M. & Kubes, P. (2018) Neutrophils and neutrophil extracellular traps in the liver and gastrointestinal system
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro