A murine model of latex allergy-induced airway hyperreactivity

Sensitization to latex proteins can cause immediate IgE mast cell-mediated reactions. Health care workers have been found to be particularly at risk because of high exposure. Latex allergy can be produced in mice as demonstrated by IgE and eosinophil responses. Thus the mouse is a potential animal model for studying this disease, but the airway response to latex sensitization in mice has not been evaluated previously. In the present study, we immunized BALB/c mice intranasally with nonammoniated latex proteins. Animals were anesthetized, and lung mechanics were evaluated plethysmographically. Changes in pulmonary conductance (G(L)) and compliance (C-dyn) were measured in response to a nonspecific challenge with methacholine or to a direct challenge with intravenous latex antigen. Latex sensitization resulted in elevated levels of IgE and latex-specific IgG(1) as well as interstitial infiltrates consistent with an allergic response. The methacholine dose-response ED50 for G(L) was 116.4 mu g for the control mice and fell significantly to 20.9 mu g for latex-sensitized mice. The ED50 calculated for C-dyn was also significantly lower after latex sensitization. The G(L) in latex-sensitized mice challenged with latex antigen fell significantly from a prechallenge value of 1.87 +/- 0.41 (S.E.) to 0.198 +/- 0.03 ml.s(-1) cmH(2)O after latex antigen challenge. The results indicate that latex-sensitized mice did exhibit increased airway reactivity in the methacholine challenge test. The latex allergic response in mice is unique in that direct challenge with latex antigen itself also resulted in a significant airway response.