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Strain differences in both immune function and behavior were observed following exposure of mice to the death of cage-cohorts. AKR/J, BALB/cN, and C3H/HeJ mice were exposed to a dead cohort for two hours at 48 hour intervals for 30 days. During this two hour period, AKR/J mice displayed intense fighting and mounting behavior. In addition, these mice attacked, cannibalized, and buried carcasses. Neither C3H/HeJ nor BALB/cN mice exhibited the complete repertoire of behaviors directed at either carcasses or cage-cohorts observed in AKR/J mice. After 15 exposures to the death of cage-cohorts, allogeneic cytotoxic T-lymphocyte (CTL) response was suppressed in AKR/J mice, but was enhanced or unchanged in C3H/HeJ and BALB/cN mice, respectively. Other immune parameters including natural killer (NK) cell activity, and lipopolysaccharide-stimulated B cell proliferation were unchanged in AKR/J mice but increased in BALB/cN mice exposed to the death of cage-cohorts for thirty days. These results suggest: 1) that both suppression of the CTL response and behaviors indicative of defensive burying in AKR/J mice may specifically be due to the loss of cage-cohorts, since they were not observed following exposure of these mice to the death of contraspecific animals; and 2) that both the behavioral repertoire and immune responses following exposure to the death of cage-cohorts may be strain dependent. This strain dependence may reflect differences in the ability to cope with the intermittent presentation of a stressor, and may explain, at least in part, variability in stress-induced changes in immune functions.

Ethanol inhibited the mitogen-induced initial increase in cytoplasmic free-calcium [Ca2+]i in mouse splenocytes. This effect was concentration-dependent, reversible, and observed at pharmacologically relevant concentrations (24-166mM). Other short-chain alcohols such as propanol, butanol, and pentanol also inhibited this mitogen-induced increase in [Ca2+]i. The potencies of these alcohols to produce this effect were highly correlated (r = 0.98, p less than 0.001) with their membrane/buffer partition coefficients. Analysis of mouse splenocyte subpopulations demonstrated that this effect was manifest in both B and T lymphocytes. Within T lymphocyte subpopulations, both CD4+ and CD8+ T cells were affected. These results suggest that the inhibition of [Ca2+]i increase may be an early event mediating ethanol-induced immunosuppression and that this may be a predisposing factor to infection and malignancies associated with alcoholism.

The kinetics of HIV-1 infection were compared among human B (DK), promonocyte (U937), T-B hybrid (CEMX174), and T (H9) cell lines. Just like H9 cells, CEMX174 cells exhibited strong syncytia induction capacity against highly HIV-1-sensitive CD4+ T cells (SupT1) and had high reverse transcriptase (RT) release in the supernatant. DK and U937 cells showed syncytia induction capacity by 72 hr, but RT activity in the culture supernatant (extracellular RT) increased much later. RT activity in cell lysates (intracellular RT) became detectable at 12-15 days. The inverted extracellular/intracellular RT ratio and syncytia induction capacity were also observed in chronically infected DK (DK-IIIB) and U937 (U937-IIIB) cell lines and subclones from U937-IIIB. Further, the coculture of H9 with DK-IIIB (which indicates no detectable extracellular RT release) showed remarkable amplification of extracellular RT with significant increase of T-B double marker hybrids (H9-DK-IIIB). Our results suggest that B cells and/or monocytes/macrophages may acquire fusing capacity against CD4+ T cells in early stages of the infection and that these cell-to-cell interactions may also lead to a reduction in the number of CD4+ T cells. Further, these T-B and T monocyte hybrids may serve as temporal sites for viral replication. These in vitro studies may provide clues to the possible immunopathological roles of HIV-1-infected B cells and monocytes/macrophages and may help in understanding the mechanisms of viral burden on an infected host.