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Treatment with anti-TNF-α and the IL-1 receptor antagonist revealed that release of IL-1β, and not TNF-α, from monocytes dominated the regulation of IL-8 release in co-cultures. However, exogenous IL-1β reduced the FGF-2 levels, strongly elevated the FGF-2-binding protein PTX3, and prevented the reduction in the number of pneumocytes induced by silica.IL-1β seems to be differently involved in the silica-induced release of IL-8 and FGF-2 in different lung cell cultures.Different co-culture models of lung cells have revealed, despite their limitations, important information about close cellular interactions and activation of signalling pathways subsequent to particle exposure [].Furthermore, monocytes are often causing marked changes in the pattern of released inflammatory mediators when interacting with epithelial lung cells.In the proximity of monocytes, pneumocytes produced less FGF-2.

In particular the M/E co-culture, but also the triplet co-culture M P/E released high levels of IL-8 upon silica exposure, indicating the influence of endothelial cells.

Chronic exposure to crystalline silica particles is associated with the development of silicosis and lung cancer in humans. This may cause cell damage and cell death, and release of oxidants or proteases [].

Attracted inflammatory cells may release potentially toxic oxygen derivates and proteolytic enzymes.

Thus, the level of IL-8 in the exposed non-contact co-culture M/E was significantly higher than M P/E, M/P and M P, at the highest silica concentration.

The release of IL-8 and FGF-2 from monocultures and co-cultures of monocytes (M), pneumocytes (P) and/or endothelial cells (E).

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The FGF-2 release seemed to increase with the silica-induced decrease in the number of pneumocytes.

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