Figure 3.

Anti-OVA IgE, but not B cells, are required for the development of airway hyperresponsiveness. Normal B10.BR (n = 12) and B cell-deficient μMt^−/− mice (n = 12) were sensitized to OVA via the airways for 10 days. A different group of μMt^−/− mice received anti-OVA IgE antibody treatment on days 4, 6, and 8 of the 10-day protocol (n = 8). Control animals were exposed to nebulized PBS (n = 8). Two days after the last challenge, in vitro airway reactivity was measured by electrical field stimulation of tracheal smooth muscle segments. Compared are the frequencies leading to 50% maximal contraction, the ES₅₀ ± SEM in hertz, from three independent experiments as a percentage of the control ES₅₀ value (100%) in (PBS) nonsensitized animals (4 ± 0.4 Hz). ∗, P < 0.02 vs. PBS; ‡, P < 0.03 vs. OVA-sensitized μMt^−/− mice without anti-OVA IgE treatment. μMt^−/− mice receiving anti-2,4,6-trinitrophenyl IgE during 10-day OVA nebulization had similar ES₅₀ levels as OVA-sensitized, nontreated μMt^−/− mice.