The neuropeptides substance P and neurokinin A are present in sensory airway nerves. Their effect on airway calibre was compared in six healthy non-smoking subjects and six asthmatic subjects. On separate days increasing concentrations (from 10(-9) to 10(-6) mol/ml) of each neuropeptide were administered by nebuliser and the airway response measured as change in specific airway conductance (sGaw). Substance P and neurokinin A caused no change in sGaw in the healthy subjects. Inhalation of substance P up to the highest concentration of 10(-6) mol/ml caused no change in sGaw in the asthmatic subjects. Neurokinin A, however, caused bronchoconstriction with a mean fall in sGaw of 48% (SEM 12%) after 5 x 10(-7) mol/ml. The onset of bronchoconstriction was rapid, but sGaw had returned to baseline values within one hour in all but one patient.

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Bacterial respiratory infections, especially with Haemophilus influenzae and Streptococcus pneumoniae, are frequently associated with an increase of airways obstruction in patients with bronchial asthma. The possible involvement of immediate hypersensitivity in this phenomenon was studied. IgE antibodies to Haemophilus influenzae (HI) and Streptococcus pneumoniae (SPn) were investigated in the serum of 190 adult patients with bronchial asthma. The IgE antibodies were measured using a solid phase radioimmunoassay method. Living bacteria were used as solid phase. A correction of the non-specific binding of IgE was necessary. IgE antibodies to one or both bacteria were present in 55 of the 190 patients (29%). Eighteen patients were sensitive to HI, 33 to SPn and four to both bacteria. Significantly more IgE antibodies to bacteria were found in patients with demonstrable IgE antibodies to various inhalant allergens. However, the IgE antibodies to one or both bacteria were also present in 22% of patients with no other demonstrable IgE mediated hypersensitivity. The total serum IgE level in patients with IgE antibodies to bacteria was not significantly higher than in patients without hypersensitivity to these bacteria. From these data we concluded that immediate hypersensitivity to bacteria may play a role in the infectious exacerbations of bronchial asthma.