Dexamethasone as a modulator of jejunal goblet cells hyperplasia during Trichinella spiralis gut infection of mice

The potentiation of parasitic infections is a recognized adverse effect of glucocorticoids after their prolonged administration. In the present study, however, the potential effects of a single small dose of glucocorticoids, dexamethasone (DEX), on suppression of the jejunal goblet cells (GC) hyperp lasia, in relation to the establishment and persistence of a primary helmin th infection, was investigated using the Trichinella spiralis/mouse model. One day prior to infection with T. spiralis, C57BL mice were treated with D EX at dose 0.1 mg/kg and necropsied for GC enumeration at 3, 4, 5 and 7 day s post-infection (p.i.) and for adult worm counts from the small intestines at 3, 4, 5, 7, 10, 14 and 21 days p.i., respectively. In addition, larval worm counts from the musculature were performed at day 35 p.i. DEX-unpretre ated T. spiralis-infected mice served as control. The control mice were nec ropsied on the same days as the tested group mice. DEX-pretreatment of mice infected with T. spiralis was found to transiently abolishes periodic-acid -Schiff (PAS)-positive GC hyperlasia normally observed following T. spirali s-infection. By contrast, DEX caused elevation of Alcian blue (ALB)-positiv e GC number during the T. spiralis-infection of C57BL mice. These findings were confirmed by a second DEX injection on day 5 p.i. Moreover, DEX-pretre atment significantly delayed adult parasite elimination from the small inte stine and the mice injected with DEX harboured significantly more larval wo rms in the musculatue than the uninjected hosts. These results suggest that DEX, administered shortly before or early after experimental infection of mice with T. spiralis, could potentiate susceptibility of host to trichinel losis, in part, in association with the suppression of PAS-positive GC hype rplasia. This also indicates that acute administration of DEX, even at the lowest dose, may induce long-lasting consequences detrimental to the infect ed host.