These suppressive effects of rIFN-γ on airway neutrophilia can be retrospectively confirmed in humans since nebulized or subcutaneously administered rIFN-γ robustly reduced BAL CXCL5 levels and neutrophils in airways of patients with idiopathic pulmonary fibrosis77 or pulmonary tuberculosis.78 Of note, despite favorable anti-neutrophilic outcomes, neither Px nor Tx rIFN-γ delivery improved airway hyper-reactivity in the acute setting of allergic asthma exacerbation tested in our studies (Figure 7H). The gene discussed is CXCL5; the disease is pulmonary tuberculosis.