Effects of Diesel Exhaust Particles on the Release of Interleukin-1 and Tumor Necrosis Factor-Alpha from Rat Alveolar Macrophages

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Abstract
The effects of diesel exhaust particles (DEP) and their components (washed dust and methanol extracts) on the release of proinflammatory cytokines, interleukin-1 (IL-1), and tumor necrosis factor-alpha (TNF-α) by alveolar macrophages (AM) were investigated. Rat AM were incubated with 0, 5, 10, 20, 50, or 100 μg/10−6 AM/mL of DEP, methanol-washed DEP, or equivalent concentrations of DEP methanol extracts at 37°C for 24 h. AM-conditioned supernatants were collected and assayed for the activities of IL-1 and TNF-α. At high concentrations, both DEP and DEP methanol extracts were shown to increase IL-1-like activity secreted by AM, whereas methanol-washed DEP had no effect. Neither DEP, methanol-washed DEP, nor DEP methanol extracts was found to stimulate the secretion of TNF-α. The effects of DEP on the release of IL-1 and TNF-α by lipopolysaccharide (LPS)- or interferon-gamma (IFN-γ)-primed AM were also studied. AM were preincubated with various concentrations of DEP for 2 h, then challenged with either 0.1 μg/mL of LPS or 5 units/mL of IFN-γ. DEP inhibited LPS-stimulated production of IL-1 and TNF-α. These inhibitory effects were attributed to the organic extracts of DEP. In contrast, stimulation of AM production of TNF-α by IFN-γ was not affected by DEP exposure. In summary, evidence that DEP enhanced the production of IL-1 by AM in vitro suggests that this proinflammatory cytokine may play a role in the pulmonary response to DEP inhalation. The suppressive response of DEP-pretreated AM to LPS stimulation may be a contributing factor to the impairment of pulmonary defense system after prolonged DEP exposure.