Sensitization to latex proteins can cause immediate IgE mast cell-mediated
reactions. Health care workers have been found to be particularly at risk b
ecause of high exposure. Latex allergy can be produced in mice as demonstra
ted by IgE and eosinophil responses. Thus the mouse is a potential animal m
odel for studying this disease, but the airway response to latex sensitizat
ion in mice has not been evaluated previously. In the present study, we imm
unized 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 measure
d in response to a nonspecific challenge with methacholine or to a direct c
hallenge with intravenous latex antigen. Latex sensitization resulted in el
evated levels of IgE and latex-specific IgG(1) as well as interstitial infi
ltrates consistent with an allergic response. The methacholine dose-respons
e 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 a
lso significantly lower after latex sensitization. The G(L) in latex-sensit
ized mice challenged with latex antigen fell significantly from a prechalle
nge 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 di
d exhibit increased airway reactivity in the methacholine challenge test. T
he latex allergic response in mice is unique in that direct challenge with
latex antigen itself also resulted in a significant airway response.