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. Author manuscript; available in PMC: 2011 Dec 1.
Published in final edited form as: Ann Allergy Asthma Immunol. 2010 Dec;105(6):437–443.e1. doi: 10.1016/j.anai.2010.09.010

Figure 3. Non-viral antigen exposure during a severe paramyxoviral infection induces airway hyperreactivity through an IgE-dependent mechanism.

Figure 3

Mice were treated as outlined in figure 1C and airway resistance to a graded methacholine challenge was measured after 3 OVA i.n. challenges. Note that all mice received 3 OVA challenges regardless of the sensitization group (PBS or OVA). (A) Wild-type mice developed significantly increased airway resistance only when they had been exposed to ovalbumin during an active viral infection (SeV-OVA). The number of mice per group were: SeV-OVA = 7, SeV-PBS = 3, UV SeV-OVA = 8, UV SeV-PBS = 8. (B) This response appeared to depend upon the high affinity receptor for IgE, since FcεRIα–/– mice did not exhibit this increased airway hyper-reactivity. The number of mice per group were: SeV-OVA = 6, SeV-PBS = 7, UV SeV-OVA = 6, UV SeV-PBS = 8. (C) This response was IgE dependent, as IgE–/– mice failed to demonstrate increased airway hyper-reactivity when given OVA during an active viral infection. The number of mice per group were: SeV-OVA = 4, SeV-PBS = 3. All data are presented as mean +/- SEM of airway resistance for each dose of methacholine. Statistical comparisons are as indicated using repeated measures ANOVA with Tukey's multiple comparison test.