These mediators include biogenic amines such as histamine and serotonin, several mast cell-specific neutral proteases (mainly tryptases and chymases) and cytokines [9].
In the CF mouse intestine several mast cell protease genes were expressed: mast cell protease 1 (mast1), mast cell protease 2 (mast2), mast cell chymase 2 (Cmalsoalso called Mcp10), mast cell carboxypeptidase A3 (Cpand, and mast cell protease-like (Mcptl) [17].
The PGs located in mast cell granules are mainly of the serglycin type, and these exert a key role in promoting the storage of numerous mediators, including histamine, serotonin and several mast cell proteases [11] [16].
Several mast cell-derived mediators, including histamine, serotonin, arachidonic acid, and mast cell proteinases have been shown to affect intestinal epithelial function, including ion channel conductance and activation/inhibition of secretion of electrolytes and mucus [8], [27], [28].
Next, the effect of polyamine depletion on the storage of several mast cell secretory granule components, i.e. histamine, serotonin, mMCP-6, mMC-CPA and β-hexosaminidase was investigated.
In line with these findings, we observed increased expression of several mast cell-associated genes, such as the mast cell chymases 1, 2 (Cma2, Cmand, and the mast cell proteases Mcpt1, Mcpt2, Mcpt4 and Mcpt9 in this model, along with the afore-mentioned Fcer1a.
In addition to Mcpt2, several other mast cell markers on the arrays were strongly upregulated in CF controls and decreased 3-20 fold in lubiprostone treated CF mice (Table 1).
In response to various stimuli, mast cells secrete a variety of bioactive substances, such as histamine and several proinflammatory cytokines, including interleukin (IL -8 and TNF.
Atopic diseases are associated with elevated levels of IgE antibodies, which bind to Fc receptors on the surface of several cell types, including mast cells and basophils.
Several groups have detected mast cells located on the ASM and demonstrated that their numbers and/or activation correlate with decline in lung function and/or severity in asthma (1, 3, 6, 7).
