Evidence 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 expression of CD 11b from 1.44 (SE 0.19) × 105 molecules of equivalent soluble fluorochrome (MESF) after air to 1.78 (SE 0.21) × 105 MESF after NO2 exposure (p =04). When corrected for nonspecific antibody binding, the difference was no longer statistically significant (p =059). No significant changes were observed in cell type, size, or expression of markers of differentiation. Exposure to 2.0 ppm NO2 for 6 h does not reduce AM expression of the 3 Fc receptors, CD11b, or CD14, and does not cause an influx of monocytes into the alveolar space immediately after exposure.
ASJC Scopus subject areas
- Health, Toxicology and Mutagenesis