Diesel particulate material binds and concentrates a proinflammatory cytokine that causes neutrophil migration.

Exposure to combustion emissions is associated with adverse health effects, but the properties of the emissions that induce these effects are not fully understood. To examine the direct effects of diesel particulate material (DPM) on alveolar epithelial cells, A549 cells were exposed to DPM. Low concentrations of DPM increased the interleukin-8 (IL-8) detected in the conditioned medium. Higher doses appeared to suppress the response, although this suppression was not related to acute DPM toxicity. In a cell-free system, incubation of IL-8 with DPM resulted in loss of immunoreactive IL-8 from the supernatant of the reaction. In contrast, carbon black did not reduce the concentration of IL-8 in the mixture. The DPM-induced loss was only weakly blocked by a large excess of bovine serum albumin (BSA). High concentrations of salts partially prevented the loss, but extraction of the soot with organic solvents had no effect. To determine biological implications, human blood neutrophils were exposed to DPM that had been preincubated with IL-8, then washed to remove free IL-8. The neutrophils changed shape in a manner suggesting directed movement toward the particles. No morphological change was observed either with carbon black that had been incubated with IL-8 or with DPM alone. These results suggest that DPM not only induces the production of IL-8 by epithelial cells, but also binds biologically active chemokine in a particle- and protein-selective manner. DPM-induced inflammatory responses may therefore be more focused or sustained as a result of this binding of inflammatory mediators by DPM.