STRESS, CONTROL AND IMMUNE REGULATION IN AN EXPERIMENTAL MODEL OF ASTHMA

Asthma is becoming more prevalent in today's world, particularly prevalent among children. Africans American children are more to susceptible to asthma than white Americans. It is becoming increasingly clear that stress is a major risk factor for asthma. Though asthma and stress has a very strong relationship, we still lack a clear understanding the of underlying mechanisms through which stress influences disease pathogenesis. Asthma has been described as psychosomatic disorder. As the pulmonary immune system is under the control of the Central Nervous system (CNS) and endocrine system, dys‐regulation in this system may be a contributing factor in immune mediated exacerbation of asthma. Our current focus is to understand how signaling events between brain, an immune privileged organ can control disease severity along the respiratory tract. To investigate the effects of stress on asthma severity, ovalbumin sensitized mice were exposed to an experimental stress paradigm involving control and uncontrolled stress conditions. Our preliminary data has shown that significant changes in behavioral patterns between the conditions that corresponded with immune dys‐regulation that corresponded immune mediated severity of asthma. We also demonstrate cortocotrophin Realeasing Hormone (CRH) expression level in the lung is associated with differences in the disease severity of asthma. Such differences suggest that stress may be a contributing factor in regulation of Antigen Presenting Cells, the key player in innate immune system. We have seen accumulation and of these cells in the lungs. We hypothesize that stress induced alteration in APC function will dictate pro‐asthmatic immune response. This link can lead us to functioning of these immune cells in the case of asthma. These findings can have the implications for treatment of Th2 mediated disease such as asthma.