IgA and IgG anti-ragweed antibodies in nasal secretions. Quantitative measurements of antibodies and correlation with inhibition of histamine release.

Total secretory IgA and specific anti-antigen E (AgE) antibodies (ab) in the IgA and IgG classes were measured in concentrated nasal washings from ragweed allergic and normal individuals by antigen binding or anti-alpha-radioimmunoassays. Virtually all the allergic patients had significant IgA (45/49) and IgG (46/49) ab to AgE in their nasal washings. By contrast, washings from most normal persons contained no measurable IgA (13/15) ab or IgG (13/15) ab to AgE. The total IgA levels in allergic washings were not significantly different from those in normal washings and they were used to standardize the ab measurements. Parenteral immunotherapy with ragweed extract increased specific nasal IgA ab from 10.6 +/- 2.7 (SEM) to 39.0 +/- 8.7 ng AgE bound/mg IgA and IgG ab from 17.2 +/- 2.6 to 65.1 +/- 7.4 ng AgE bound/mg IgA (P less than 0.001 for both classes). The ratio of IgA:IgG ab was not affected by therapy, and for treated patients, there was no correlation (rs + 0.32, P greater than 0.1) between nasal IgG ab and serum IgG ab. These results suggest that at least part of the nasal IgG ab is produced locally. Blocking activity in the nasal washings was measured by inhibition of histamine release and was found to correlate directly (rs + 0.85, P less than 0.001) with binding activity for AgE. Some washings from normal persons caused slight inhibition of histamine release but others caused enhancement. Nasal washings were fractionated by passage over Sephadex G-200. Inhibition of histamine release by dilutions of the IgA-rich and IgG-rich fractions correlated well with binding activity in these fractions. None of these results support the hypothesis that allergic individuals are deficient in secretory IgA or secretory ab responses. These results, however, are in keeping with the theory that hay fever occurs in a high-responder population which is genetically able to respond to low doses of inhalant antigens.