Gene program of neutrophil recruitment and tissue injury based on gene expression and in vitro data

A gene program of neutrophil recruitment and tissue injury based on gene expression and in vitro data. Molecules in black text represent those added to the pathway based on microarray data, while molecules/genes in blue text have supportive inmmunohistochemical and/or in vitro data. Immune complexes and/or mycobacterial components may activate FcRs and TLRs to induce pro-inflammatory cytokines such as IL-8 and IL-1β. IL-1β in combination with IFN-γ induce E-selectin expression on endothelial cells, resulting in the first step of neutrophil recruitment, adhesion and rolling along the endothelial wall. These steps are inhibited by thalidomide. Neutrophil interaction with ICAM-1 as well as other integrin-mediated activators results in arrest and activation. Glycosaminoglycans such as heparan sulfate and extracellular proteins such as plasminogen activator inhibitor 1 promote the presentation of chemokines such as IL-8 on the surface of the endothelium to mediate neutrophil activation and chemotaxis, inhibited by secretory component. As part of the innate immune response to microbial infection, the local recruitment of neutrophils may lead to tissue injury as host defense pathways are executed.

Publication

Integrated pathways for neutrophil recruitment and inflammation in leprosy. () Delphine J. Lee, et al. J Infect Dis. ;201(4):558-569. Figure: F7. Homo sapiens

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