Changes in numbers and types of mast cell colony-forming cells in the peritoneal cavity of mice after injection of distilled water: evidence that mast cells suppress differentiation of bone marrow-derived precursors

Abstract

Two different types of cells in the peritoneal cavity of mice produce mast cell colonies in methylcellulose. “Large” mast cell colonies are produced by bone marrow-derived precursors resembling lymphoid cells by light microscopy (L-CFU-Mast), whereas “medium” and “small” mast cell colonies are produced by morphologically identifiable mast cells (M-CFU- Mast and S-CFU-Mast, respectively). In the present study we eradicated peritoneal mast cells by intraperitoneal (IP) injection of distilled water. The regeneration process was investigated to clarify the relationship between L-CFU-Mast, M-CFU-Mast, and S-CFU-Mast. After injection of distilled water, M-CFU-Mast and S-CFU-Mast disappeared, but L-CFU-Mast increased, and then M-CFU-Mast and S-CFU-Mast appeared, suggesting the presence of a hierarchic relationship. When purified peritoneal mast cells were injected two days after the water injection, the L-CFU-Mast did not increase. In the peritoneal cavity of WBB6F1-+/+ mice that had been lethally irradiated and rescued by bone marrow cells of C57BL/6-bgJ/bgJ (beige, Chediak-Higashi syndrome) mice, L-CFU-Mast were of bgJ/bgJ type, but M-CFU-Mast and S-CFU-Mast were of +/+ type. The injection of distilled water to the radiation chimeras resulted in the development of bgJ/bgJ-type M-CFU-Mast and then S-CFU-Mast. The presence of mast cells appeared to suppress the recruitment of L-CFU- Mast from the bloodstream and to inhibit the differentiation of L-CFU- Mast to M-CFU-Mast.

Expression of a B‐cell‐restricted isoform of CD45 is associated with maturity in rat serosal and connective‐tissue mast cells

“…Adoptive transfer of purified OX33 + and OX33 ) subsets of SMCs showed formally that the OX33 ) cells acquire the OX33-reactive CD45 isoform with time. By contrast, there was no reversion from the OX33 + phenotype under these conditions, but because differentiation may be regulated by resident SMCs, 18 further studies are required to test this possibility in recipients that have been depleted of MCs. The origin of the newly formed SMCs was not explored, but evidence in mice indicates that there is regeneration from both nongranular MC precursors and granulated SMCs.…”

“…The origin of the newly formed SMCs was not explored, but evidence in mice indicates that there is regeneration from both nongranular MC precursors and granulated SMCs. 18 It will be of interest to examine whether mature SMCs down-regulate the expression of OX33-reactive CD45 in an MCdepleted environment, whether the OX33 ) subset or the OX33 + subset is more effective in regenerating MCs and whether the decline in responsiveness to growth factors that has been reported with maturation is associated with switching to the OX33-reactive CD45 phenotype. 33 Cells labelled with the monoclonal anti-FceRI in SRT of normal hind paws were found also to be heterogeneous in expression of OX33-reactive CD45 (Fig.…”

“…Resident peritoneal MCs were depleted by hypotonic lysis, as described in mice by Kanakura et al 18 While under general anaesthesia, the experimental group received 15 ml of sterile distilled water (DW) by intraperitoneal (i.p.) injection, while controls received 15 ml of sterile physiological saline.…”

“…To examine the hypothesis that OX33 ) FceRI + SMCs are the least mature and that the OX33-reactive CD45 isoform is up-regulated during SMC maturation, we adapted the method used by Kanakura et al 18 in mice to ablate MCs in the peritoneal cavity. By 24 hr after injection of physiological saline, the total number of peritoneal cells had increased (data not shown) as the result of an acute inflammatory exudate of neutrophilic granulocytes ( Fig.…”

“…17 Thus, the usual approaches for measurement of cell turnover in vivo are not practical and the estimates that are available have been obtained by observing rates of reconstitution of MC numbers after chemical or physical depletion of resident populations. 17,18 Another approach for studying the dynamics of CTMCs in normal or pathological tissues has been to estimate the proportions of immature and mature cells based on levels of GAG sulphation. 19 However, these estimates rely on histochemical differences in staining (e.g.…”