02404nas a2200457   4500000000100000008004100001260001600042653002100058653001500079653003000094653001100124653001700135653002100152653002200173653001200195653002300207653003100230653002800261653004400289653001800333653002400351653000900375653001600384653002500400100001100425700000900436700001300445700001300458700001400471700001700485700001400502700001200516700001000528700001400538245008000552856006600632300001100698490000800709520121500717022001401932       2010                            d  c2010 Feb 1510aCluster Analysis10aE-Selectin10aGene Expression Profiling10aHumans10aInflammation10aInterferon-gamma10aInterleukin-1beta10aleprosy10aModels, Biological10aMycobacterium lepraemurium10aNeutrophil Infiltration10aOligonucleotide Array Sequence Analysis10aReceptors, Fc10aSignal Transduction10aSkin10aThalidomide10aToll-Like Receptor 21 aLee DJ1 aLi H1 aOchoa MT1 aTanaka M1 aCarbone R1 aDamoiseaux R1 aBurdick A1 aSarno E1 aRea T1 aModlin RL00aIntegrated pathways for neutrophil recruitment and inflammation in leprosy.  uhttp://jid.oxfordjournals.org/content/201/4/558.full.pdf+html  a558-690 v2013 a<p>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 1beta (IL-1beta). In vitro activation of Toll-like receptor 2 (TLR2), up-regulated in ENL lesions, triggered induction of IL-1beta, which together with interferon gamma 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.</p>  a1537-6613