Hemophilus pertussis vaccine injected into normal rat skin produced local edema lasting several days. Four to 6 days later the injected site became severely inflamed. When uninjected skin was challenged 5 to 28 days after the initial injection, severe inflammation developed at the site of challenge within 12 to 24 hours. This secondary hypersensitive response was elicited by a dose of vaccine which produced little or no initial or delayed inflammation in a normal rat. Specific cutaneous hypersensitivity to a particulate antigen (i.e. typhoid vaccine) or a soluble antigen (human or rabbit gamma globulin) developed when rats were injected with a mixture of the antigen and pertussis vaccine. Pertussis vaccine mixed with typhoid vaccine did not enhance circulating agglutinin formation to typhoid vaccine. Cutaneous hypersensitivity to pertussis vaccine was passively transferred to normal rats by lymph node cells but not with serum from hypersensitive rats. Sensitization with pertussis vaccine did not enhance the edema-producing activity of histamine, serotonin, or 48/80 given subcutaneously. Mast cells in areas of hypersensitive inflammation were not damaged appreciably. The hypersensitive inflammation was not inhibited by treatment with anti-serotonin and antihistaminic drugs. Hypersensitive rats "depleted of mast cells" responded to challenge with pertussis vaccine with severe inflammation though their response to 48/80 was depressed. Hypersensitive rats treated with x-irradiation showed decreased hypersensitive inflammation though they responded normally to 48/80 and histamine.

These studies failed to demonstrate a role for circulating antibody in the cutaneous hypersensitive inflammation produced in the rat by pertussis vaccine. Furthermore, the findings indicated that the cutaneous hypersensitive inflammation is not mediated by tissue serotonin and/or histamine.

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