Date of Award

Summer 1990

Document Type


Degree Name

Master of Science (MS)


Biological Sciences



Committee Director

Robert E. Ratzlaff

Committee Member

R. James Swanson

Committee Member

Christopher J. Osgood

Call Number for Print

Special Collections LD4331.B46 C38


The direct stimulation of sensory nerves or the intradermal injection of neuropeptides triggers a cutaneous inflammatory response that involves the degranulation of mast cells. These neurogenic inflammatory reactions are physiologically similar to IgE-mediated hypersensitivity responses, which also depend on mast cells. Although non-antigenic stimuli distinguish neurogenic from IgE-mediated inflammation, the similarity of their effector stages suggested that peripheral nerves may also participate in lgE-mediated responses. To examine this hypothesis, IgE responses were elicited in denervated skin. A murine model was developed where the footpad was denervated by surgically removing a 2 mm segment of the sciatic nerve, proximal to the tibial and common peroneal branch. The other hind leg received either sham surgery or no surgery (untreated). One week after surgery, cutaneous inflammation was induced in denervated footpads with a monoclonal IgE and its antigen, and compared to responses in sham and untreated control footpads. IgE-induced swelling was significantly reduced by approximately one-third in denervated footpads of both passively sensitized and immunized mice. In denervated footpads passively sensitized with lgE, reduced swelling responses were observed over a range of local IgE doses, and were not dependent on the route of sensitization. In denervated footpads of immunized animals, significantly reduced swelling responses were measured against two different antigens. This reduction in IgE-mediated inflammation detected in denervated footpads was not due to hyporesponsive blood vessels, because denervated footpads responded normally to the vasoactive mediators histamine and serotonin. Hyporesponsiveness to IgE in denervated skin was not the result of the desensitization of mast cells, or to a change in mast cell number. These findings indicate that peripheral nerves contribute significantly to IgE-mediated inflammation, demonstrating in vivo the existence of a neurogenic component during IgE responses in the skin.


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