MAST-CELLS THAT RESIDE AT DIFFERENT LOCATIONS IN THE JEJUNUM OF MICE INFECTED WITH TRICHINELLA-SPIRALIS EXHIBIT SEQUENTIAL-CHANGES IN THEIRGRANULE ULTRASTRUCTURE AND CHYMASE PHENOTYPE

Whether or not a nontransformed, mature mouse mast cell (MC) or its co mmitted progenitor can change its granule protease phenotype during in flammatory responses, has not been determined. To address this issue, the granule morphology and protease content of the MC in the jejunum o f BALB/c mice exposed to Trichinella spiralis were assessed during the course of the infection. Within 1 wk after helminth infection of the mice, increased numbers of MC appeared in the crypts at the base of th e villi, and by wk 2 the number of MC throughout the villi increased b y similar to 25-fold. Shortly after the peak of the mastocytosis, the intraepithelial population of MC disappeared, followed by a progressiv e loss of lamina propria MC. The presence of stellate-shaped granules containing crystalline structures in intraepithelial MC at the height of infection and the retention of such granules with fragmented crysta ls in lamina propria MC during resolution of the mastocytosis suggest that MC migrate during the various phases of the inflammation. As asse ssed by immunohistochemical analyses of serial sections, predominant c hymase phenotypes were observed at the height of the infection in the muscle that expressed mouse MC protease (mMCP) 5 without mMCP-1 or mMC P-2 and in the epithelium that expressed mMCP-1 and mMCP-2 without mMC P-5. Accompanying these two MC populations were transitional forms in the submucosa that expressed mMCP-2 and mMCP-5 without mMCP-1 and in t he lamina propria that expressed mMCP-2 alone. These data suggest that jejunal MC sequentially express mMCP-2, cease expressing mMCP-5, and finally express mMCP-1 as the cells progressively appear in the submuc osa, lamina propria, and epithelium, respectively. In the recovery pha se of the disease, MC sequentially cease expressing mMCP-1, express mM CP-5, and finally cease expressing mMCP-2 as they present at the tips of the villi, the base of the villi, and the submucosa, respectively. That MC can reversibly alter their protease phenotypes suggests that a static nomenclature with fixed functional implications is inadequate to describe MC populations during an inflammatory process within a par ticular tissue.