Stress and allergic pulmonary inflammation

The interactions between stress and allergic pulmonary inflammation are not well understood. Experiments were conducted utilizing the ovalbulmin (OVA) sensitization and aerosol challenge to induce allergic pulmonary inflammation in mice and stimulate the T helper (Th2) milieu immunity in female Balb/c mice. An Ovalbumin (OVA) sensitization and aerosol challenge model was utilized. The first study utilized an amphetamine withdrawal model as the stressor. There were no significant immune x stress interactions. An additive effect was observed for some Th2 cytokines and lung inflammation. The second study evaluated lipopolysaccahride challenge and forced swim test (FST), effects on mouse plasma corticocosterone levels at 20, 50, and 80 min after the start of exposure. FST treated mice, 50 minutes after exposure had the highest levels of corticosterone. Control mice also had elevated levels of corticosterone compared to literature baseline levels. The third study attempted to establish a time when full lung inflammation occurred. Sampling times included 0, 12, 24, 36 and 48 h after aerosol challenge. Mice harvested 0 to 24 h post allergen exposure had the most complete inflammatory response (not significant). The final study examined the effects of the FST on allergic pulmonary inflammation using the OVA induced allergy mouse model. Th2 cytokines in BAL fluid were elevated among allergic mice, the stressor reduced IL-5 and IL-6 concentrations in allergic mice, while the stressor alone (non-allergic) caused an increase in IL-4 and IL-10.