Abstract

AbstractEvidence from both animal and human investigations suggests that exposure to nitrogen dioxide (NO2,), a common air pollutant, increases susceptibility to respiratory infections. In animals, alveolar macrophage (AM) antimicrobial functions are impaired following NO2 exposure. We sought to determine whether exposure to NO2 in humans causes an influx of less mature AM into the alveolar space and/or results in decreased expression of AM surface markers important in antimicrobial defense. Eight human volunteers underwent bronchoalveolar lavage (BAL) immediately following 6-h exposures to 2.0 ppm NO2 or filtered air. AM expression of receptors for the Fc component of immunoglobulin (Ig), complement receptor 3 (CD11b), and monocyte marker CD14 were assessed using imniunofluorescence staining and flow cytometry. The use of internal fluorescence standards reduced analytical variability by 32% and allowed detection of relatively small changes in cell surface antigen expression. We observed an increase in AM...

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