Production of tumor necrosis factor, interleukin-6 and prostaglandin E2 by LPS-stimulated rat bone marrow macrophages after thermal injury: Effect of indomethacin

Ogle, Cora K.; Guo, Xiang; Szczur, Kathy; Hartmann, Sharon; Ogle, James D.

doi:10.1007/bf01534558

Cited by 29 publications

(16 citation statements)

References 41 publications

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“…While indomethacin, which inhibits PGE 2 synthesis, resulted in a small reduction in the ability of IL-6 plus IL-6sR to stimulate aromatase activity, it is possible that this effect is mediated by the compound inhibiting IL-6 production (Ogle et al 1994).…”

Section: Resultsmentioning

confidence: 99%

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The regulation of aromatase activity in breast fibroblasts: the role of interleukin-6 and prostaglandin E2.

Singh

Purohit²,

Ghilchik³

et al. 1999

Endocrine-Related Cancer

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Prostaglandin E 2 (PGE 2 ) and cytokines, such as interleukin-6 (IL-6) or tumour necrosis factor α (TNFα) can regulate aromatase activity. In the present study we have compared their abilities to stimulate aromatase activity in fibroblasts derived from 'normal' breast adipose tissue proximal to a tumour or breast tumours. PGE 2 , TNFα and IL-6 plus its soluble receptor (IL-6sR) all increased aromatase activity in these cells. Basal aromatase activity and the degree of aromatase stimulation by these factors were greater in fibroblasts derived from 'normal' breast tissue than from breast tumours. The ability of IL-6+IL-6sR to increase aromatase activity was only marginally reduced by the PG synthesis inhibitor, indomethacin, indicating that IL-6+IL-6sR does not appear to act via induction of PG synthesis. The ability of PGE 2 to stimulate aromatase activity in fibroblasts derived from 'normal' breast tissue was potentiated by IL-6sR suggesting that PGE 2 may act via induction of IL-6. This was confirmed by measurement of IL-6 in conditioned medium collected from these cells. A significant increase in IL-6 concentrations was detected in conditioned medium collected from cells treated with PGE 2 . It is concluded that in some fibroblasts PGE 2 may exert part of its regulatory effect Endocrine-Related Cancer (1999) 6 139-147 on breast tissue aromatase activity via induction of IL-6.

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Section: Resultsmentioning

confidence: 99%

“…As a small reduction in aromatase activity was detected when IL-6+IL-6sR plus indomethacin were used in combination to treat cells, this could suggest that IL-6+IL-6sR can stimulate PGE 2 synthesis, although only to a small degree. However, there is evidence that indomethacin can also inhibit IL-6 secretion in some cells (Ogle et al 1994).…”

Section: Resultsmentioning

confidence: 99%

The regulation of aromatase activity in breast fibroblasts: the role of interleukin-6 and prostaglandin E2.

Singh

Purohit²,

Ghilchik³

et al. 1999

Endocrine-Related Cancer

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“…Further, IL-I and have been demonstrated to induce kinin B1 receptor in vitro (Deblois et al, 1988). As systemic treatment with LPS is capable of upregulating certain cytokine genes of macrophage, neutrophils and fibroblasts in vivo (Ulich et al, 1992;Cockfield et al, 1993;Huleihel et al, 1993), through steroidal (Geiger et al, 1993;Ochalski et al, 1993;Pang et al, 1994), and nonsteroidal-sensitive mechanisms (Ochalski et al, 1993;Ogle et al, 1994), it seems apparent that the induction of B1 receptormediated oedema formation in the rat paw after LPS treatment is mediated by cytokine release. Together, these findings are consistent with the view that the induction of B. receptors in animals pretreated with LPS plays an important role in maintaining the chronic inflammatory processes, as already reported in hyperalgesic and some inflammatory models Bhoola et al, 1992;.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of B₁ receptor mediating des‐Arg₉‐BK‐induced rat paw oedema by systemic treatment with bacterial endotoxin

Campos

Souza

Calixto

1996

British J Pharmacology

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1 The effect of pretreatment with bacterial endotoxin (LPS, 10 pg, i.v., 24 h) on the bradykinin B1 and B2 receptor-induced oedema in the rat paw, and the interaction of B,-mediated responses with other inflammatory mediators, was investigated. 2 Intraplantar (i.pl.) injection of the selective B1 agonist, des-Arg9-BK (DABK, 100 nmol) in naive animals pretreated with the angiotensin converting enzyme inhibitor, captopril caused a small increase in paw volume (0.04 + 0.003 ml, mean + s.e.mean, n = 6), while the B2-selective agonist, tyrosine8-bradykinin (T-BK, 3 nmol) induced marked oedema (0.36 + 0.02 ml). However, i.pl. injection of DABK (3-300 nmol) in rats pretreated with LPS (24 h beforehand) resulted in a marked dose-and time-related increase in paw volume, with mean ED50 of 24.1 nmol. In contrast, oedema caused by T-BK (3 nmol) was reduced by 79 + 4% in animals treated with LPS when compared with naive animals. 3 Oedema caused by prostaglandin E2 (PGE2, 10 nmol) was unaffected by LPS treatment, while oedema induced by histamine (100 nmol), 5-hydroxytryptamine (5-HT, 10 nmol) and substance P (SP, 3 nmol) was reduced (P<0.05).4 The selective B, antagonist, des-Arg9[Leu8]-BK (100-300 nmol), produced dose-dependent inhibition of DABK (100 nmol)-induced paw oedema in LPS-treated animals with mean IC50 of 134 nmol, while the selective B2 antagonists, Hoe 140 and NPC 17731 (each 10 nmol), had no effect.5 Treatment of animals with dexamethasone (0.5 mg kg-', s.c.) 24 or 48 h prior to LPS injection resulted in a graded inhibition of DABK (100 nmol)-induced oedema formation (58+3 and 82+2%, respectively), and almost reversed to control value oedema formation induced by T-BK (3 nmol) in LPSpretreated rats. Cycloheximide (1 mg kg-1, s.c.) or indomethacin (2 mg kg-1, i.p.) pretreatment 24 and 1 h prior to LPS injection, respectively, markedly inhibited DABK (100 nmol)-induced paw oedema (98+2 and 50+4%, respectively). 6 Intraplantar injection of submaximal dose of DABK (10 nmol) in LPS-treated rats produced modest paw oedema (0.09+0.03 ml). However, i.pl. injections of PGE2, prostacyclin (PGI2), calcitonin-generelated peptide (CGRP), SP, 5-HT, or platelet activating factor (PAF) (each 1 nmol), which alone caused little or no paw oedema, resulted in a potentiation of the DABK-induced oedema. The increases in paw volume (in ml) were: PGE2 + DABK (0.31 + 0.03), PG12 + DABK (0.39 + 0.02), CGRP + DABK (0.35+0.04), DABK+SP (0.33+0.04), DABK+5-HT (0.40+0.02) and DABK+PAF (0.38+0.016) ml. In contrast, histamine (1 nmol) was ineffective in potentiating the response to DABK. 7 The selective B1 receptor antagonist, DALBK (100-300 nmol), produced dose-dependent inhibition of paw oedema potentiation induced by co-injection of DABK and other mediators with mean ID50s (nmol) of: 180, 160, 139 and 135 in the presence of PGE2, PGI2, SP and 5-HT, respectively.

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“…Since macrophages are a major source of PGE 2 during inflammation (40) and since they also have receptors for and respond to this eicosanoid (41), the PGE 2 generated by macrophages may regulate cytokine synthesis in an autocrine fashion (in contrast to paracrine regulation achieved through adding exogenous PGE 2 to cells). Previous studies have implicated a positive association between endogenous PGE 2 production and IL-6 synthesis in vitro (14,42,43), and animal models of chronic inflammation show that PGE 2 is a stimulator of IL-6 production in vivo (14, 25, 42, 44 -46).…”

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confidence: 97%

Regulation of Macrophage Cytokine Production by Prostaglandin E2

Williams

Shacter

1997

Journal of Biological Chemistry

185

109

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Prostaglandin E 2 (PGE 2 ) modulates a variety of physiological processes including the production of inflammatory cytokines. There are two cyclooxygenase (Cox) enzymes, Cox-1 and Cox-2, that are responsible for initiating PGE 2 synthesis. These isozymes catalyze identical biosynthetic reactions but are regulated by different mechanisms in the cell. This report examines differences in the roles of Cox-1 and Cox-2 in regulating cytokine synthesis in macrophages. We employed agents that selectively modulate the activity of each isozyme and measured their effects on synthesis of interleukin (IL)-6, IL-1, and tumor necrosis factor-␣ by peritoneal macrophages. Among these three cytokines, only IL-6 synthesis was stimulated by production of endogenous PGE 2 . This effect was specifically linked to activation of Cox-2 and not Cox-1. The specificity derives, partly, from the timing of the production of PGE 2 following stimulation of each isozyme and from induction of ancillary signals that control the response to PGE 2 . The experimental findings demonstrate that the effects of Cox-1 and Cox-2 activity on macrophage IL-6 synthesis are segregated. This provides a mechanism for IL-6 to be induced selectively during inflammation.

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Production of tumor necrosis factor, interleukin-6 and prostaglandin E2 by LPS-stimulated rat bone marrow macrophages after thermal injury: Effect of indomethacin

Cited by 29 publications

References 41 publications

The regulation of aromatase activity in breast fibroblasts: the role of interleukin-6 and prostaglandin E2.

The regulation of aromatase activity in breast fibroblasts: the role of interleukin-6 and prostaglandin E2.

Upregulation of B₁ receptor mediating des‐Arg₉‐BK‐induced rat paw oedema by systemic treatment with bacterial endotoxin

Regulation of Macrophage Cytokine Production by Prostaglandin E2

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Production of tumor necrosis factor, interleukin-6 and prostaglandin E2 by LPS-stimulated rat bone marrow macrophages after thermal injury: Effect of indomethacin

Cited by 29 publications

References 41 publications

The regulation of aromatase activity in breast fibroblasts: the role of interleukin-6 and prostaglandin E2.

The regulation of aromatase activity in breast fibroblasts: the role of interleukin-6 and prostaglandin E2.

Upregulation of B1 receptor mediating des‐Arg9‐BK‐induced rat paw oedema by systemic treatment with bacterial endotoxin

Regulation of Macrophage Cytokine Production by Prostaglandin E2

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Upregulation of B₁ receptor mediating des‐Arg₉‐BK‐induced rat paw oedema by systemic treatment with bacterial endotoxin