The mast cell is an essential effector cell in allergic inflammation through its capacity to respond to IgE dependent activation with release of both preformed and newly generated mediators. Mast cells also participate in the modulation of physiolo...
The mast cell is an essential effector cell in allergic inflammation through its capacity to respond to IgE dependent activation with release of both preformed and newly generated mediators. Mast cells also participate in the modulation of physiologic processes, but the role of mast cell in these processes is still unclear. Recently, the number of structurally defined chemoattractants for leukocytes has greatly increased, owing to largely to the identification of the chemokine superfamily. Chemokines are small proteins with molecular weights in the range of 8 to 12 kD and inducible in a number of pathophysiologic precesses.
This study is aimed to examine the pattern of expression of chemokines in human mast cell line (HMC-1). HMC-1 were treated with PMA/ionophore and/or LPS and their induction of mRNA and protein were investigated by RT-PCR and ELISA. Messenger RNA of IL-8 , the representative CXC chemokine, was induced after PMA/ionophore treatment. All of the CC chemokines tested except eotaxin were induced after PMA/ionophore treatment and MIP-1α and MIP-1β were expressed their mRNA moderately in the resting state. CCR1, CXCR2, CXCR3 and CXCR4 were expressed in all test group regardless of activation. CCR3 was expressed only at 3 hours of activation. CCR2 and CXCR1 were not expressed in mast cell line. Production of chemokine protein was not detected in resting state and increased significantly after 3 hours of activation with PMA/ionophore. The effect of LPS treatment was negligible. MCP-1 protein was always produced without activation and accumulated in a time-dependent manner. These data suggest that the expression of mRNA and protein of chemokines and chemokine receptors are regulated transcriptionally and translationally.
Human mast cell may respond to various stimuli by producing chemokines and their receptors to regulate their function and may act autonomously or through other inflammatory cell that they recruited.