Macrophages synthesise and release prostaglandins in response to inflammatory stimuli

Humes, John L.; Bonney, Robert J.; Pelus, Louis M.; Dahlgren, Mary Ellen; Sadowski, S.; Kuehl, Frederick A.; Davies, P.L.

doi:10.1038/269149a0

Cited by 548 publications

(167 citation statements)

References 11 publications

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“…Other work from our laboratory has demonstrated that monocytes directly resorb both devitalized bones by a mechanism which is not mediated by the action of osteoclasts (25) and live bones through an osteoclast-mediated mechanism which is prostaglandin-dependent (26). There is also other evidence which suggests that monocytes and macrophages synthesize and release PGs (27)(28)(29), collagenase (30), and hydrolytic enzymes (31), which are all capable of resorbing bone or degrading bone matrix. It is also possible that circulating mononuclear cells may transform or differentiate into osteoclasts (32).…”

Section: Discussionmentioning

confidence: 99%

Monocytes regulate osteoclast-activating factor production by releasing prostaglandins.

Yoneda¹,

Mundy²

1979

The Journal of Experimental Medicine

129

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Osteoclast-activating factor (OAF), a powerful stimulator of osteoclastic bone resorption, is released by peripheral blood mononuclear cells on exposure to phytohemagglutinin (PHA) or a specific antigen to which the leukocytes have been previously exposed. Both lymphocytes and monocytes are required in the leukocyte population for OAF release to occur. In this study we examined the relationship between the lymphocyte and monocyte in OAF production. Biological activity, as a result of OAF, was assessed by a bioassay based on the release of previously incorporated 45Ca from fetal rodent long bones in organ culture. We found that an enriched lymphocyte population depleted of monocytes by serial adherence does not release OAF after stimulation with PHA, although the cells are activated as assessed by [3H]thymidine and 3H-amino acid incorporation. When conditioned media harvested from adherent cells which did not contain OAF was added to the enriched lymphocytes, OAF release occurred. Media harvested from adherent cells which were cultured with indomethacin (10 microM), an inhibitor of prostaglandin synthesis, did not permit OAF release by activated lymphocytes. When PGE1 and PGE2 (0.1 microM) were added exogenously to the enriched lymphocyte population, OAF release occurred after stimulation with PHA. These results indicate that, (a) the activated lymphocyte is the cell or origin of OAF, (b) prostaglandins produced by monocytes are necessary for OAF production by activated lymphocytes, and (c) monocyte prostaglandins can influence bone resorption indirectly by regulating OAF production as well as directly by osteoclast activation. The interactions of OAF and prostaglandins at bone resorbing sites may be important in inflammatory and neoplastic diseases associated with bone destruction.

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Section: Discussionmentioning

confidence: 99%

Monocytes regulate osteoclast-activating factor production by releasing prostaglandins.

Yoneda¹,

Mundy²

1979

The Journal of Experimental Medicine

129

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“…The presence of this enzyme was also noted by Sahu and Lynn (16) in human and by Masliah et al (17) in rat BAL fluids. Its activity was also shown to increase in cells during the inflammatory reactions induced by exposure to toxicants such as silica or asbestos (13,18). However, many questions remain unresolved regarding this enzyme.…”

Section: Discussionmentioning

confidence: 99%

Biochemical components of bronchoalveolar lavage in early experimental asbestosis of the sheep: phospholipase A2 activity, prostaglandin E2 and proteins.

Sirois¹,

Drapeau²,

Bégin³

1983

Environ Health Perspect

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Biochemical analyses of bronchoalveolar lavage (BAL) supernatants of sheep treated with weekly intratracheal instillations (for 6 months) of saline, 2 mg, or 128 mg of asbestos (chrysotile B; UICC) were performed. Our results showed that proteins (either total or its various components) and phospholipase A2 activity were unchanged in the low exposure group as compared to controls. However, in the high exposure group, with histopathological evidence of early asbestosis, there were significant increases in total proteins, albumin, a2-globulin, f3-and y-globulins as well as phospholipase A2 activity of BAL fluid. Prostaglandin E2 activity was significantly increased in both low and high dose groups. These changes in protein and lipid components of BAL following asbestos exposure constitute early indices of lung inflammatory reactions which may contribute to the development of asbestosis.

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“…We have no evidence to suggest that in generalized inflammatory diseases the plasma concentrations of PGE2, PGE2 metabolites, or other metabolites of arachidonic acid are elevated, although the tissue levels may be high at localized sites of inflammation. On the other hand, inflammatory stimuli appear to enhance the synthesis and release of PGE2, and possibly other metabolites of arachidonic acid, from macrophages (33). Thus it is possible that certain inflammatory stimuli lead to elevations in plasma of acute phase reactants, including ceruloplasmin and haptoglobin, via a pathway which depends on arachidonic acid metabolism.…”

Section: Weeksmentioning

confidence: 99%

Acute phase reactants ceruloplasmin and haptoglobin and their relationship to plasma prostaglandins in rabbits bearing the VS2 carcinoma.

Voelkel¹,

Levine²,

Alper³

et al. 1978

The Journal of Experimental Medicine

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Results of a series of studies on the cause of the hypercalcemia that occurs in mice bearing the HSDM~ fibrosarcoma (1-6) and in rabbits carrying the VX2 carcinoma (7-9) have led us to conclude that these two tumors synthesize and secrete large amounts of prostaglandin E2 (PGE2) into plasma. ~ PGE~ is a potent bone resorption-stimulating agent in vitro (2, 10), and this prostaglandin and its metabolites are found in elevated concentrations in the plasma of tumor-bearing animals (2,3,(6)(7)(8)11). Because of the rapid clearance and metabolism of PGE2, measurements in plasma of the metabolite, 13,14-dihydro-15-keto-PGE2(PGE2-M), give a more accurate estimate of PGE~ secretion than do measurements of the primary prostaglandin itself (6,8,11,12). Studies on the time-course of the development of elevated plasma calcium concentrations and hyperprostaglandinemia, as well as investigations using two inhibiters of prostaglandin synthesis, indomethacin (1-3, 7) and hydrocortisone (6,8,13), support the hypothesis that the hypercalcemic syndrome in these tumor-bearing animals is due to the secretion of PGE2 by the tumor. A similar pathophysiologic mechanism may explain in part the hypercalcemia that occurs in certain patients with cancer (14-16).The present investigation was initiated because of the observation that the plasma from rabbits bearing the VX~ carcinoma became faintly blue about I wk after tumor implantation, and this color increased markedly and became intense by 3-4 wk. The time-course of the appearance and increase in the blue color in plasma was similar to that which we had previously noted for PGEz-M. We therefore undertook to identify the blue material in plasma and to examine the relationship of its increase to prostaglandin metabolism. Our findings indicate that the material is ceruloplasmin, that its rise correlates closely with plasma concentrations of PGE2-M, and that beth PGE2-M and ceruloplasmin increase in the plasma of tumor-bearing rabbits before the development of hypercalcemia.

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Macrophages synthesise and release prostaglandins in response to inflammatory stimuli

Cited by 548 publications

References 11 publications

Monocytes regulate osteoclast-activating factor production by releasing prostaglandins.

Monocytes regulate osteoclast-activating factor production by releasing prostaglandins.

Biochemical components of bronchoalveolar lavage in early experimental asbestosis of the sheep: phospholipase A2 activity, prostaglandin E2 and proteins.

Acute phase reactants ceruloplasmin and haptoglobin and their relationship to plasma prostaglandins in rabbits bearing the VS2 carcinoma.

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