Cement-related particles interact with proinflammatory IL-8 chemokine from human primary oropharyngeal mucosa cells and human epithelial lung cancer cell line A549.

Epidemiological studies have shown that respirable exposure to emitted cement particulate matter is associated with adverse health risk for human. The underlying mechanisms, however, are poorly understood. To examine the effect of cement, nine blinded cement-related particulates (<10 μm) were assessed with regard to their induction of the proinflammatory cytokines IL-6 and IL-8 in human primary epithelial cells (pEC) from oropharyngeal mucosa as well as from nonsmall-cell lung carcinoma (non-SCLC) cells A549. It was demonstrated that the cement specimens did not act cytotoxic as assessed by the lactate dehydrogenase (LDH) assay. The basal and IL-1β-induced IL-8 expression was suppressed, in contrast to an unchanged IL-6. At the transcript level the basal and induced IL-6 and IL-8 gene expression was not influenced by cement dust. To discover the mechanism by which cement influenced the IL-8 expression the following experiments were performed. Submerse exposure experiments have shown that the release of IL-8 was suppressed by cement dust. Furthermore, the incubation of IL-8 with cement-related specimens under cell-free condition led to a loss of immunoreactive IL-8. An immunological masking of IL-8 by free soluble components of respiratory epithelial cells was excluded. Thus, the decrease of IL-8 protein content after cement exposure seems to be a result of the adsorption of IL-8 protein to cement particles and the inhibition of IL-8 release. In conclusion, due to absent cytotoxic and inflammatory effects of cement-related specimens in both human pEC and A549 cell models it remains open how cement exposure may lead to the respiratory adverse effects in humans.