Mast cells (MCs) play a key role in the pat hogenesis of allergic diseases. Tissue MCs are originated from hematopoietic ste m cells in bone marrow. In recent years, it was reported that human mast cells c ould be differentiated from stem cells of umbilical cord blood. In this review, we summarize the development in this novel area.

AIM: To investigate the actions of trypsi n on the secretion of monocyte chemoattractant protein-1 (MCP-1) from human lung e pithelial cells. METHODS: A549 cells were cultured in a 12-well culture plate. Th e challenge was performed by addition of various concentrations of trypsin or tr ypsin inhibitor into each well, respectively. After 2 h, 8 h or 16 h, the reacti ons were terminated by removal of the supernatant from each well. A sandwich ELI SA was used to determine the levels of MCP-1 in supernatants. RESULTS: Following 16 h incubation, trypsin was able to induce c oncentration-dependent secretion of MCP-1. As low as 3 ?g/L trypsin was able to induce MCP-1 release from epithelial cells, and the maximum of accumulated rele ase of MCP-1 was observed with 100 ?g/L trypsin, which was 3 fold more than bas eline release. However, trypsin at 300 ?g/L did not induce significant MCP-1 se cretion. Soybean trypsin inhibitor (SBTI) inhibited trypsin-induced MCP-1 secret ion, but ? 1-antitrysin (? 1-AT) did not. The time course showed that the actions of trypsin initiated at 2 h and reached their peak at 16 h. CONCLUSION: Trypsin is a potent secretogogue of MCP-1 release fr om cultured human lung epithelial cells, and itself action can be inhibited by S BTI.

AIM: To investigate the ability of leupeptin, TLCK and lactoferrin on tryptase release from human colon mast cells. METHODS: Human mast cells were dispersed from colon tissue with collagenase and hyaluronidase, and were challenged with stimulus for 15 min at 37 ℃. Tryptase concentrations were measured with a sandwich ELISA procedure. RESULTS: Leupeptin, TLCK and lactoferrin were not able to provoke significant tryptase release from human colon mast cells. But they were able to inhibit anti-IgE and calcium ionophore (CI)-induced tryptase release in a concentration-dependent manner. Preincubation of inhibitors of leupeptin and TLCK with cells for 20 min before challenging with anti-IgE failed to enhance their inhibitory actions. The extent of inhibition by leupeptin was increased when colon mast cells were preincubated for 20 min before CI being added. However, the same treatment failed to improve the action of TLCK. CONCLUSION: We found for the first time that leupeptin, TLCK and lactoferrin were able to inhibit anti-IgE and calcium ionophore-induced tryptase release from human colon mast cells, which may indicate a potential of a novel therapy for the treatment of inflammatory bowel disease or other mast cells-related diseases.

Since the discovery of mast cells (MCs) in 1878, MCs have long been recognised to be the key effector cells in allergic reactions. However, little is known about their roles in defending microorganisms. In this review, the recent research progress in the roles of MCs, in the body defence against bacterial and viral infection, in pathogen recognition mechanisms and in inflammatory mediator release are discussed.

Objective To investigate the expression of protease activated receptors(PARs)in mast cells.Methods Reverse transcription polymerase chain reaction(RT-PCR),flowcytometry and immunofluorescent cell staining were used to detect the expression of PARs in mast cell lines P815 and MC/9 at the levels of protein and mRNA.Results Both the P815 and MC/9 of mast cell lines expressed PAR-1,PAR-2,PAR-3 and PAR-4 at either protein or mRNA level.Conclusion The expression of all the four PARs in mast cells were detectable,which may be of significance for the further study on the function of PARs in mast cells.

Tryptase,a multifunctional inflammatory mediator,is mainly secreted by activated mast cells and can initiate the development of many diseases.Accordingly the plasma tryptase level is increased with the degranulation of the mast cells,and the detection of the changes in its serum level may provide valuable evidence for the clinical diagnosis and treatment of related diseases.

As an important mediator of allergic inflammation, mast cell tryptase is involved in the induction of hypersensitivity, infiltration of inflammatory cells and tissue remodeling in respiratory tract. The effects of tryptase inhibitors on the actions of tryptase show further the potential of tryptase in the pathogenesis of asthma and its inhibitors in the treatment of asthma.

Transforming growth factor-?(TGF-?)was reported to be increased in asthma in some studies. Accumulation of TGF-? in airway promotes smooth muscle cell mitogenesis and hyperplasia, and induces fibroblast and myofibroblast and smooth muscle proliferation as well as increase in protein synthesis in connective tissue(such as collagen deposition on the reticular basement membrane). The autocrine induction of collagen expression by smooth muscle may contribute to the thickening of the reticular basement membrane, irreversible fibrosis and remodeling seen in the airways in some asthmatics. TGF-? is considered to be a major fibrogenic cytokine. It can increase smooth muscle mass and lead to severe bronchial obstruction in an asthma attack.

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Many newly discovered interleukins have been implicated to play an important role in the pathogenesis of the allergic diseases, for example, human interleukin (IL)-17, a T-cell derived cytokine; interleukin (IL)-18, an interferon (IFN)-gamma-inducing cytokine; interleukin (IL)-23, produced by activated dendritic cells, and interleukin (IL)-25, a recently described T helper 2 (Th2) cell-derived cytokine. Understanding their characteristic and roles in diseases may help us to know better the mechanism of the allergic diseases and develop the strategy for treating the disease. [