Regulation of human lung fibroblast glycosaminoglycan production by recombinant interferons, tumor necrosis factor, and lymphotoxin.

Synergistic, additive, and antagonistic effects of interleukin‐1β, tumor necrosis factor α, and γ‐interferon on prostaglandin e, hyaluronic acid, and collagenase production by cultured synovial fibroblasts

“…In another study with synovial cells, TNFa was reported to be slightly more effective than IL-1 in stimulating PGE, and collagenase release (13); however, this may have been due to the use of murine cytokines, whose effects on human synovial cultures differ from those of human cytokines (31). Minor, if any, effects of y I F N have been reported in other studies of PGE production by human synovial cells (19,3 l), collagenase production by human synovial cells (34), dermal fibroblasts (33, and bone cells (36), and HA or glycosaminoglycan production by lung (37) and dermal (35) fibroblasts.…”

“…A number of common proteins are induced, particularly by IL-1 and TNFa, and these proteins may be responsible for the overlapping cell regulatory actions of these cytokines (39). Specific effects of IL-1 on HA production appear to involve an activated HA synthetase activity (37,40); however, other metabolic effects, such as increased intracellular precursor pools of UDP-glucuronic acid and UDP-N-acetylglucosamine, may also be involved (8,37). For PGE synthesis induced by IL-1 and TNFa in human synovial fibroblasts, increased substrate availability of arachidonic acid caused by an elevation in phospholipase A, activity is implicated (25).…”

Tumour necrosis factor: a cytokine with multiple biological activities

“…In fact, TNF induces fibroblasts to grow and to produce IL-1 , colony stimulating factors (Zucali et al, 1987), interferon beta-2 (Van Damme et al, 1987) and glycosaminoglycans (Elias et al, 1988). TNF has been found to be capable of stimulating collagenase and PGE2 production by isolated synovial cells and dermal fibroblasts (Dayer et al, 1985).…”

Dietary lipids and the inflammatory response

“…Similarly, the increased rate of non-secretory protein synthesis by liver of rats given endotoxin or IL-1 is not prevented by ibuprofen (Kunkel et al 1987). Furthermore, increases in glycosaminoglycan synthesis in lung fibroblasts stimulated with TNF were unaffected by indomethacin (Elias et al 1988). Thus, alternative mechanisms have to be sought for the modulatory effects of fats on the responses of visceral protein synthesis to cytokines.…”