Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.59 (MIP)
 4,906 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human chymase induced release of interleukin-8 (IL-8) in human EoL-1 cells that had been differentiated into eosinophil-like cells with butyric acid. The chymase-induced IL-8 production was specific in that other cytokines/chemokines examined were not induced. Human chymase also increased mRNA for IL-8 in the differentiated EoL-1 cells, showing involvement of mRNA synthesis. The chymase-induced IL-8 release was inhibited by pertussis toxin as well as U0126 (an inhibitor for extracellular signal-regulated kinase pathway) and SB203580 (p38 inhibitor), suggesting that the chymase-induced IL-8 production is mediated by G protein-coupled receptor and mitogen-activated protein kinases. Mouse mast cell protease-4 (mMCP-4), a mouse chymase, induced macrophage-inflammatory protein-2 (MIP-2), a mouse homologue for IL-8, in mouse eosinophils in vitro. Intradermal injection of mMCP-4 not only induced skin edema but increased MIP-2 content and neutrophil number at the injection site. Taken together, our findings demonstrate that mast cell chymase may contribute to the interaction between eosinophils and neutrophils by inducing IL-8/MIP-2 in eosinophils at allergic inflamed sites.
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PMID:Mast cell chymase induces expression of chemokines for neutrophils in eosinophilic EoL-1 cells and mouse peritonitis eosinophils. 1669 53

Recent evidences indicate an important role of tissue inflammatory responses by innate immune cells in allograft acceptance and survival. Here we investigated the role of mast cells (MC) in an acute male to female skin allograft rejection model using red MC and basophil (RMB) mice enabling conditional MC depletion. Kinetic analysis showed that MCs markedly accelerate skin rejection. They induced an early inflammatory response through degranulation and boosted local synthesis of KC, MIP-2, and TNF. This enhanced early neutrophil infiltration compared to a female-female graft-associated repair response. The uncontrolled neutrophil influx accelerated rejection as antibody-mediated depletion of neutrophils delayed skin rejection. Administration of cromolyn, a MC stabilizer and to a lesser extent ketotifen, a histamine type I receptor antagonist, and absence of MCPT4 chymase also delayed graft rejection. Together our data indicate that mediators contained in secretory granules of MC promote an inflammatory response with enhanced neutrophil infiltration that accelerate graft rejection.
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PMID:Mast Cell Degranulation Exacerbates Skin Rejection by Enhancing Neutrophil Recruitment. 3051 67