Yue, Simon Christopher; (2011) Isolation and characterisation of mast cells from the prostate and other locations in normal and inflamed tissue. Doctoral thesis (Ph.D.), University College London.

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Abstract

The present study has shown that the majority of rat prostatic mast cells counterstained with safranin O but a significant proportion were also sensitive to formaldehyde fixation. This indicates that they may be intermediate in phenotype between the traditional connective tissue and mucosal mast cell extremes. Consistently, the cells released histamine on challenge such polyamines, which is characteristic of connective tissue mast cells, but were refractory to DSCG and nedrocromil sodium, which is typical of mucosal mast cells. Cells isolated from sites distal to the locus of inflammation in nematode infected rats were generally more responsive than normal cells to calcium ionophores and immunological stimuli. In contrast, cells did not show any differences in responsiveness towards polybasic compounds after sensitisation. Moreover, mast cells isolated from the lungs were more responsive towards immunological stimuli after nematodes infection but, in contrast, they were generally less responsive to both calcium ionophores and polybasic compounds. These data suggest that the induction of airway inflammation with nematodes may led to mast cell hyperplasia in the lungs and that the newly recruited cells may be immature or of the mucosal phenotype as judged by their Histochemical and functional characteristics. The synergistic effect of polybasic compounds on IgE induced histamine release was more pronounced in connective tissue than mucosal type mast cells. The level of enhancement produced by a single dose of a given polybasic compound increased as the histamine release induced by anti-IgE decreased. Human lung mast cells and basophil leukocytes did not respond to polyamines alone. Our study also showed that the enhancement by bradykinin of anti-IgE induced histamine release is due to an increased production of IP3 and a corresponding elevated rise in intracellular Ca2+.

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