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. Author manuscript; available in PMC: 2011 Nov 4.
Published in final edited form as: J Immunol. 2010 Jul 19;185(4):2525–2535. doi: 10.4049/jimmunol.1000286

Figure 4. RV infection of OVA-sensitized and -challenged mice induces eotaxin-1-mediated airways cholinergic responsiveness.

Figure 4

A. Mice were anesthetized and endotracheally intubated, and changes in respiratory system resistance to nebulized methacholine measured using the FlexiVent system (Scireq, Montreal, CA). Four days after infection, RV-infected OVA mice demonstrated significantly higher airways responses than all other groups at methacholine doses of 10 and 20 mg/ml. B. Measurement of viral copy number from lungs of PBS/RV and OVA/RV treated mice 1 day post infection. OVA/RV treatment significantly reduced viral copy number by 1 log. (N= 5 mice per group, bars represent mean ± SEM, *different from respective sham group, p<0.05; †different from respective PBS group, P<0.05 one-way ANOVA.) C. Selected RV-infected, OVA-sensitized and -challenged mice were given two systemic injections of rabbit anti-mouse eotaxin-1. Additional mice were treated with the isotype control antibody. Mice given anti-eotaxin displayed reduced tissue eosinophils 4 days after infection. D. Neutralizing antibody and isotype control-treated mice were administered increasing doses of aerosolized methacholine. Treatment with anti-eotaxin-1 significantly reduced airway cholinergic responsiveness compared to the IgG-treated group. (Bars represent mean ± SEM, *different from respective sham group, †different from IgG group, P<0.05, one-way ANOVA.)