We show that 14C11 was effective in suppressing each of the outcomes that were exacerbated by rhinovirus infection superimposed on a model of ovalbumin induced allergic airway inflammation, including HRV-induced exacerbation of total cellular, neutrophilic and lymphocytic airway inflammation, as well as Th2 (IL-4 and IL-5) and pro-inflammatory (IL-6) cytokine and neutrophil (CXCL1) and eosinophil (eotaxin) recruiting chemokine release. This evidence concerns the gene CCL11 and inflammatory response.