Phenotypic and functional assessments of immune status in the rat spleen following acute heroin treatment.

Heroin use is associated with an increased incidence of several types of infections, including HIV. Yet few studies have assessed whether heroin produces pharmacological alterations of immune status that might contribute to the increased rate of infections amongst heroin users. The present study investigated whether a single administration of heroin to rats produces dose-dependent alterations in functional measures of immune status and in the distribution of leukocyte subsets in the spleen. The results showed that heroin produces a dose-dependent, naltrexone-reversible suppression of the concanavalin A-stimulated proliferation of T cells, lipopolysaccharide-stimulated proliferation of B cells, production of interferon-gamma and cytotoxicity of natural killer (NK) cells in the spleen. Heroin's suppressive effect on NK cell activity results in part from a heroin-induced decrease in the relative number of NKR-P1A(hi) CD3- NK cells in the spleen. Heroin also decreases the percent of a splenic granulocyte subset, the CD11b/c+ HIS48(hi) cells, whose function currently is unknown. In contrast, heroin does not alter relative numbers of CD4+ CD3+ T cells, CD8+ CD3+ T cells, CD45+ B cells, NKR-P1A(lo) CD3+ T cells, CD11b/c+ ED1+ (or CD11b/c+ HIS48-) monocytes/macrophages or CD11b/c+ ED1- (or CD11b/c+ HIS48+) total granulocytes in the spleen. Collectively, these findings demonstrate that heroin produces pharmacological effects on functional and phenotypic measures of immune status.