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Integrated Pathways for Neutrophil Recruitment and Inflammation in Leprosy
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Integrated Pathways for Neutrophil Recruitment and Inflammation in Leprosy
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Journal Article
Integrated Pathways for Neutrophil Recruitment and Inflammation in Leprosy
2010
Overview
Neutrophil recruitment is pivotal to the host defense against microbial infection, but it also contributes to the immunopathology of disease.We investigated the mechanism of neutrophil recruitment in human infectious disease by means of bioinformatic pathways analysis of the gene expression profiles in the skin lesions of leprosy. In erythema nodosum leprosum (ENL), which occurs in patients with lepromatous leprosy and is characterized by neutrophil infiltration in lesions, the most overrepresented biological functional group was cell movement, including E-selectin, which was coordinately regulated with interleukin 1β (IL-1β). In vitro activation of Toll-like receptor 2 (TLR2), up-regulated in ENL lesions, triggered induction of IL-1β, which together with interferon γ induced E-selectin expression on and neutrophil adhesion to endothelial cells. Thalidomide, an effective treatment for ENL, inhibited this neutrophil recruitment pathway. The gene expression profile of ENL lesions comprised an integrated pathway of TLR2 and Fc receptor activation, neutrophil migration, and inflammation, providing insight into mechanisms of neutrophil recruitment in human infectious disease.
Publisher
The University of Chicago Press,University of Chicago Press,Oxford University Press
Subject
/ Biological and medical sciences
/ Fundamental and applied biological sciences. Psychology
/ Genes
/ Humans
/ Interferon-gamma - biosynthesis
/ Interferon-gamma - immunology
/ Interleukin-1beta - biosynthesis
/ Interleukin-1beta - genetics
/ Interleukin-1beta - immunology
/ Leprosy
/ Lesions
/ Mycobacterium lepraemurium - isolation & purification
/ Neutrophil Infiltration - drug effects
/ Neutrophil Infiltration - genetics
/ Neutrophil Infiltration - immunology
/ Oligonucleotide Array Sequence Analysis
/ Receptors, Fc - biosynthesis
/ Signal Transduction - drug effects
/ Toll-Like Receptor 2 - biosynthesis
/ Toll-Like Receptor 2 - genetics
