My research centers around the hypothesis that the peripheral nervous system is directly involved in the processes of inflammation. This hypothesis is being studied primarily in the central airways and sympathetic ganglia. We are addressing this in a multidisciplinary fashion using pharmacological, electrophysiological, biochemical, and anatomical methodologies. In the isolated airways, we have found that inflammatory mediators released as a consequence of antigenic stimulation leads to an increase in the excitability of the parasympathetic neurons. The mechanisms underlying this increase in "reactivity" of the neurons include membrane depolarization, increases in membrane resistance, and a decrease in the accommodative properties of the neurons. We have also found that inflammatory mediators can significantly increase the excitability of airway afferent fibers in the airways. These and other findings support the concept that the inflammatory process may directly influence the regulatory control provided by the autonomic and sensory nervous system in the airways.