Association of Mononuclear Cells and Eosinophils with Airway Resistance and Responsiveness in Rat Pulmonary Inflammatory Responses
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Pediatric Allergy & Immunology
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To evaluate the association of various leukocytes with pulmonary resist ance and methacholine responsiveness, we induced pulmonary eosi-nophil-rich inflammation in IgE-sensitized (ovalbumin) Sprague Dawlcy rats. Sensitized rats were challenged with either relevant (OA) or irrele vant antigen by tracheal insufflation a) with no other treatment, b) in conjunction with intravenous Sephadex beads pretrcatment, or c) with antigen coupled covalently to Sepharose heads. About 24 h after antigen challenge, respiratory system resistance (Rrs), response to aerosolized methacholine, and pulmonary histopathology were evaluated. Challenge with OA, insufflation with Sepharose, and treatment with i. v. Sephadex all independently increased inflammatory cell infiltrates, but the combi nation of OA with the other agents did not significantly enhance the inflammatory response over OA alone. Interactive stepwise regression techniques were utilized to identify correlates for Rrs and methacholine responsiveness. Mononuclear cell score was a significant predictor (p < 0.1) for Rrs, and insufflation of Sepharose had a significant inde pendent effect on Rrs (p=. 01) above that predicted by mononuclear cell infiltrates. Conversely, eosinophil score and neutrophil score were not significant predictors for Rrs, and challenges with antigen or Sephadex had no significant independent effect on Rrs beyond that predicted from mononuclear cell infiltrates. Eosinophil score was the only significant histological predictor for methacholine responsiveness (p <0.001). Chal lenges with Sephadex, antigen and Sepharose did not significantly change methacholine responsiveness independently of the changes asso ciated with eosinophil infiltrates. These findings suggest that mononucle ar cells and eosinophils contribute to increases in airway resistance and responsiveness, respectively, following the induction of pulmonary inflammation by both allergic and non-allergic stimuli.