154 STRESS EFFECTS ON IMMUNITY AND ASTHMA IN TH1- AND TH2-STIMULATED MICE.

Introduction Asthma is a chronic airway disease characterized by inflammation and bronchial hyperresponsiveness and may be associated with remodeling. Acute asthma exacerbation remains a leading cause of hospitalization in both pediatric and adult populations. Stress is a well-known anecdotal cause of acute asthma exacerbation. Objectives The objective of the present study was to investigate the effect addictive chemical withdrawal stress in a mouse model of allergic immune events and pulmonary inflammation. Materials and Methods Control BALBc mice received saline immunizations and no aerosol. Th1-treated mice were immunized with ovoalbumin (OVA). Th2 nice were immunized and then aerosolized with OVA. Chemical withdrawal stress was obtained with simultaneous administration of intraperitonial amphetamine and then withdrawal (the stress experience). Each combination of control, Th1, and Th2 were cross-classified with stress and no stress. Bronchoalveolar lavage (BAL) fluid and plasma were assessed for Th1 and Th2 cytokines. Pulmonary histopathology was examined for signs of allergic inflammation. Results Pulmonary inflammatory was observed in response to OVA sensitized and aerosolized mice (Th2). Compared with control mice, both Th1 and Th2 treatment groups had elevated neutrophil:lymphocyte ratio and IgE concentrations in plasma. BAL IL-5 was elevated among mice receiving OVA immunization and aerosol compared with Th1 and control mice. Stressed Th2 mice tended to have greater BAL concentrations of IL-5 compared with nonstressed Th1 mice and Th2-stressed mice had significantly higher IL-5 than control and Th1 mice both in stress and control conditions. Conclusions Few studies have described the effect of stress on allergic pulmonary inflammation in spite of the observation that stress exacerbates asthma. Our findings indicate that (a) our Th2 model was a meaningful model of asthma, (b) immunization (Th1) may have effects on the immune system that are similar to stress, and (c) that stress may exacerbate Th2 cytokine responses and clinical signs of asthma. Findings from this study and others will lead to unique strategies for prevention and treatment of acute asthma.