6533b824fe1ef96bd127fed3

RESEARCH PRODUCT

Modulation of IL-1?, IL-6, IL-8, TNF-?, and TGF-? secretions by alveolar macrophages under NO2 exposure

subject

description

Activated alveolar macrophages (AMs) secrete interleukine (IL)1β, IL-6, IL-8, tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β), whose inflammatory and fibroblast-activating characteristics may play a role in the maintenance of pulmonary inflammatory processes and subsequent fibrosis. Human AMs were transferred to a gas cylinder and exposed to NO2 in concentrations ranging from 0.1 to 0.5 ppm in synthetic air for 30 min at 37°C. AMs were fixed on a polycarbonate membrane and placed on culture medium. A culture was established, with the exposed AM (nonstimulated or stimulated with 1 μg/ml lipopolysaccharide [LPS]), and the remaining cells were used to determine the cytokines. IL-1β, IL-6, and IL-8 were quantified by commercial enzyme-linked immunosorbent assay kits (ELISA kits). TNF-α was determined with a “sandwich” ELISA, using the biotin-streptavidin system. NO2 exposure of nonstimulated AM did not result in changes in IL-1β, IL-6, TNF-α, and TGF-β release, compared to the situation with control experiments. Exposure for 30 min to NO2 induced a significant decrease of LPS-stimulated IL-1β, IL-6, IL-8, and TNF-α (p < .05). The release of TGF-β was not significantly affected by NO2 exposure. Cytotoxicity of AM was checked by trypan blue exclusion, with values ranging from 1.3 to 3.0%. NO2 exposure of LPS-stimulated AM resulted in a functional impairment of AM after NO2 exposure regarding IL-1β, IL-6, IL-8, and TNF-α. Neither the spontaneous nor the stimulated release of TGF-β were influenced by NO2.