The inhibition of fibroblast proliferation caused by rIL-1 plus rTNF was, at least partially, mediated by fibroblast PGE2 production and was the result of the ability of rIL-1 and rTNF to synergistically stimulate fibroblast prostaglandin production. In contrast, the effects of rIFN-7 and rTNF in combination were not mediated by fibroblast prostaglandin production. When viewed together, these studies demonstrate the existence of a complex network of interacting cytokines that provides stimulatory and inhibitory signals for fibroblast function. In this network, the effect of a cytokine varies depending on the state of activation of the target cell, the presence of other cytokines in the local microenvironment, and the ability of the target cell to produce bioactive autocoids such as prostaglandins. buy asthma inhalers
Cell-cell communications in biology are usually bidirectional. This led us to hypothesize that fibroblasts not only receive instructions from mononuclear cells but that they, in turn, feed back to regulate mononuclear cell function. To test this hypothesis, we determined whether cytokine stimulated fibroblasts produce important regulators of inflammation. Our studies demonstrated that rIL-1 and rTNF individually stimulate fibroblast IL-l-a and IL-6 production. Importantly, they also showed that IL-l-a and IL-6 production by human lung fibroblast is synergistically augmented when fibroblasts are incubated with rIL-1 and rTNF in combination.
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