In conventional rats, we have previously demonstrated that corticosteroid treatment caused macrophage engulfment and destruction of intestinal mucosal mast cells and eosinophils by 24 h without evidence of local tissue destruction, inflammation or secretion of rat mast cell protease II. As the growth and survival of these cells appear to be dependent on factors derived from T lymphocytes, we examined the response in congenitally athymic rnu/rnu rats and euthymic rnu/+ rats 35 days after parasitic infection. Rats were injected intraperitoneally with 1 mg dexamethasone and sections of jejunum were examined at 0, 7, 13 and 24 h. The numbers of mucosal mast cells significantly decreased in both groups and became less than 30% of the original values at 24 h. Tissue mast cell protease decreased similarly. However, protease in serum did not increase and there were no inflammatory changes at any time. The numbers of eosinophils also rapidly decreased and became less than 20% at 24 h in both rnu/rnu and rnu/+ rats. By electron microscopy, we saw granular changes (fusion) in mast cells and nuclear changes (apoptosis) in eosinophils by 7 h after corticosteroid in athymic rats. Macrophage engulfment of these cells was observed at 7 and 13 h. Our results suggest that inflammatory cell depletion by macrophages is not dependent on suppression of typical thymus-derived T lymphocytes, and may be due either to direct effects of steroids on the cells themselves, or indirectly upon cells other than T cells which normally supply maintenance and growth factors for them.

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