Cytokine Networks in the Regulation of Inflammation and Fibrosis in the Lung (Part 3)

In: Pulmonary function

9 Nov 2012

Since fibroblasts in vivo are frequently exposed to more than one cytokine, we investigated the effects of various combinations of rIL-1, rTNF, and rIFN-7 on fibroblast proliferation. These studies demonstrated that cytokines in combination have quantitatively and qualitatively different effects than they have individually. Individually, rIL-1 (a and (5) and rTNF each stimulated fibroblast proliferation. However, when combined, they caused a dose-dependent inhibition in fibroblast proliferation (Table 1 and data not shown). ventolin inhalers

This inhibition was, at least partly, mediated by fibroblast prostaglandin production since it was reversed when fibroblast prostaglandin production was blocked with indomethacin and reproduced with exogenous prostaglandin E2 (PGE2) (data not shown). The inhibition resulted from the ability of the rIL-1 and rTNF to synergistically stimulate fibroblast prostaglandin E2 production with the PGE2 feeding back in an autocrine or paracrine fashion to inhibit fibroblast proliferation (data not shown). Combining rIFN-7 with rTNF also resulted in a synergistic inhibition of fibroblast proliferation (Table 1). However, this inhibition was not mediated by fibroblast prostaglandin production since indomethacin did not reverse the inhibition of fibroblast proliferation caused by rIFN-7 plus rTNF and rIFN-7 and rTNF in combination did not alter fibroblast prostaglandin production.

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