Learning occurs with repetitions of inspiratory loading.

human and murine allergic airway inflammation. While its effector function is incompletely understood, our preliminary experiments lead us to propose that IL-16 is a naturally occurring modulator of Th2 cell-mediated airway inflammation. Prior experiments have demonstrated that IL-16 interferes with antigen recognition and Th2 cytokine production by CD4 cells. We tested the hypothesis that IL-16 down-regulates Th2-mediated immune responses in the murine ovalbumin sensitization and challenge model. T cells isolated from ovalbumin-sensitized mice that had been treated systemically with IL-16 had markedly diminished antigen-induced IL-5 release (Fig 1). IL-16 had a similarly inhibitory effect on the response to aerosol allergen challenge. There was lower BAL eosinophilia (mean 14 10 vs 163 10 per sample) and airway inflammation from mice treated intratracheally with IL-16 prior to each ovalbumin challenge. In order to correlate physiologic with inflammatory responses, we measured airway reactivity to methacholine in ovalbumin-sensitized and challenged mice treated with IL-16 or vehicle. Ovalbumin-induced airway hyperresponsiveness (AHR) was diminished by intratracheal IL-16 treatment (Fig 2). These results were corroborated with the finding of augmented AHR in ovalbumin-sensitized and challenged IL-16 knockout mice compared to wt littermate control mice. We conclude that there are corresponding immunomodulatory effects of IL-16 on allergic airway inflammation in vivo to those seen on CD4 T cells in vitro. These observations suggest that IL-16 and related compounds may offer a novel therapeutic approach to allergic airway inflammation and AHR seen in asthma.