Prostaglandin and thromboxane production by human and guinea-pig macrophages and leucocytes

Morley, John E.; Bray, M.A.; Jones, R. W.; Nugteren, D.H.; Dorp, D. A. van

doi:10.1016/s0090-6980(79)80044-1

Cited by 188 publications

(48 citation statements)

References 21 publications

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“…Monocytes were the major leucocytes producing PGs, confirming previous work (26). Significant differences in the absolute leucocyte PG production were not detected between controls and mothers of AGA and SGA babies, despite the latter group being zinc depleted and there being a weak correlation between PG production and PMN zinc status.…”

Section: Discussionsupporting

confidence: 87%

Prostaglandin Production and Zinc Depletion in Human Pregnancy

et al. 1985

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ABSTRACT. An association between zinc depletion and intrauterine growth retardation might occur through disturbed prostaglandin (PG) synthesis. The zinc content and PG metabolism of leucocytes from control, nonpregnant women and mothers 24-48 h after delivery, were measured and related to fetal growth and maternal smoking. Mothers of small for gestational age babies had lower polymorphonuclear and mononuclear cell zinc contents than mothers of appropriate for gestational age babies or nonpregnant controls. Monocytes were the major leucocytes producing PGs. Mothers of small for gestational age babies had higher PGE2:Fk ratios than mothers of appropriate for gestational age babies. PGFk production and PGE2:Fk ratio were correlated with tissue zinc status. Monocytes from nonsmokers tended to produce more PGs than those from smokers but the differences were not significant. Mild maternal zinc depletion is not significantly sufficient to alter absolute PC production, but is associated with altered differential production of PGs in human leucocytes. Zinc depletion or malnutrition may contribute to intrauterine growth retardation by affecting placental and/or umbilical PG production. (Pediatr Res 19: 697-700,1985) Abbreviations PC, prostaglandin SGA, small for gestational age AGA, appropriate for gestational age IUGR, intrauterine growth retardation PMN, polymorphonuclear MN, mononuclear MC, monocyte IUGR is an important cause of perinatal morbidity and mortality in developed, as well as developing, countries, and in both animals ( l,2) and man (3,4) occurs with maternal zinc depletion. Zinc is present in many metalloenzymes and is essential for DNA and RNA synthesis and, therefore, protein accumulation and growth (5). It is also important in the structure and function of biomembranes (6). An interaction between zinc and essential fatty acids has been postulated (7,8), but aberrations in the metabolism of essential fatty acids attributed to zinc deficiency may be due to the accompanying reduced food intake (9). Zinc may be necessary for at least two stages in essential fatty acid Received December 4, 1984; accepted March 5, 1985. Correspondence to Dr. Karen Simmer, Gastrointestinal Laboratory, Rayne Institute, St. Thomas' Hospital, London SE1 7EH, London.Supported by Action Research, Nest16 Nutrition Foundation, and the Special Trustees of St. Thomas' Hospital. metabolism, namely the conversion of linoleic acid to y-linolenic acid, and the mobilization of dihommogammalinolenic acid for the synthesis of 1 series PGs. Zinc may also be important in the conversion of dihommogammalinolenic acid to arachidonic acid and for mobilization of arachidonic acid for 2 series PG formation (10). One of the immediate consequences of zinc depletion may be altered PG metabolism and, as PGs are important in placental function and fetal growth (1 1), an association between zinc depletion and IUGR might occur through disturbed PG synthesis.Leucocytes are readily available and produce prostaglandins (12). Their zinc content is a goo...

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Section: Discussionsupporting

confidence: 87%

Prostaglandin Production and Zinc Depletion in Human Pregnancy

et al. 1985

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“…m It has been proposed that platelets play a role in the development of inflammation by generating oxygenation products of arachidonic acid (Silver, Bills & Smith, 1978) although there is evidence that the inflammatory response is not diminished in thrombocytopaenic animals (Ubatuba, Harvey & Ferreira, 1975). The detection of thromboxane in inflammatory exudates has been offered as support for the theory that platelets are an important source of cyclooxygenase in inflammation (Silver et al, 1978 (Higgs, McCall & Youlten, 1975) and TXA2 (Higgs, Bunting, Moncada & Vane, 1976) and there is evidence that thromboxane is the predominant cyclo-oxygenase product synthesized by all types of circulating leukocyte (Morley et al, 1979). A characteristic of acute inflammation is the emigration of PMN leukocytes into inflamed tissues.…”

Section: Discussionmentioning

confidence: 99%

The source of thromboxane and prostaglandins in experimental inflammation

Higgs

Moncada

Salmon

et al. 1983

British J Pharmacology

115

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1Although cyclo-oxygenase products have been detected at inflammatory sites the tissue of origin remains uncertain. 2 Inflammatory exudates were collected from rats 4, 6, 8, 12 or 24 h after subcutaneous implantation of carrageenin-impregnated sponges.3 Concentrations of the cyclo-oxygenase products prostaglandin E2 (PGE2), 6-oxo-PGF,,, and thromboxane B2 (TXB2) in inflammatory exudates and serum (obtained from blood clotted at 370 C) were measured by specific radioimmunoassays. 4 TXB2 concentrations in exudates increased to about 100 ng ml-l at 8 h but decreased to less than 20 ng ml-l after 24 h. PGE2 concentrations increased from 4-12 h and remained between 80 and 120 ng ml 'from 12 -24 h. 6-oxo-PGF,,, had the same time course as that of PGE2 but concentrations were approximately one third of PGE2 values. 5 TXB2 concentrations in serum from thrombocytopaenic rats were less than 5 % of control values.Thrombocytopaenia did not affect TXB2, PGE2 or 6-oxo-PGFI,e concentrations or total leukocyte numbers in inflammatory exudates. 6 Methotrexate-induced neutropaenia did not affect serum TXB2 concentrations but cyclooxygenase products (including TXB2) in 6 h inflammatory exudates were reduced by 60-95 %. 7 Colchicine (1.0 mg kg-' s.c.) prevented leukocyte accumulation in sponge exudates and this was accompanied by a reduction in TXB2, PGE2 and 6-oxo-PGFI, concentrations at 6 h.8 These results indicate that platelets are the source of TXB2 in clotting blood but do not contribute to cyclo-oxygenase activity in experimental inflammation. The results also suggest that migrating leukocytes are the major source of thromboxane and to a lesser degree prostaglandins in acute 6 h inflammatory exudates.

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“…Stimulation of human and animal eosinophils with various soluble and nonsoluble agents leads to the formation of various arachidonic acid-derived lipids, including LTC 4 [63,69,[115][116][117], PGE [118,119], prostaglandin F 1 (PGF 1 ) and TxA 2 [64,[119][120][121][122][123], PGD 2 and prostaglandin F 2α (PGF 2α ) [64,123]. In addition, eosinophils have been shown to synthesize large amounts of PAF [117,[124][125][126].…”

Section: Oxygen Metabolitesmentioning

confidence: 99%

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part I)

Kroegel¹,

Virchow²,

Luttmann³

et al. 1994

Eur Respir J

129

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P Pu ul lm mo on na ar ry y i im mm mu un ne e c ce el ll ls s i in n h he ea al lt th h a an nd d d di is se ea as se e: : t th he e e eo os si in no op ph hi il l l le eu uc co oc cy yt te e ( (P Pa ar rt t I I) ) ABSTRACT: Increasing evidence has accumulated to suggest that eosinophils play a key role in the pathogenesis of asthma and other pulmonary diseases by damaging infiltrated bronchial tissue and lung parenchyma. The first part of this review on eosinophils describes the cellular characteristics and properties of the cell, which help in understanding its role in disease. The article focuses on origin, maturation and differentiation of the eosinophil, its morphological and phenotypical properties, as well as its preformed and newly generated mediators of inflammation. The cause and putative significance of eosinophil heterogeneity in respect to function and density will also be discussed. In addition, the naturally occurring mediators through which eosinophils are activated and communicate with other inflammatory cells are outlined.The first part closes with new aspects of eosinophil recruitment from the circulation into perivascular tissue, including nonselective and putative selective adhesion mechanisms and chemotaxis.

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Prostaglandin and thromboxane production by human and guinea-pig macrophages and leucocytes

Cited by 188 publications

References 21 publications

Prostaglandin Production and Zinc Depletion in Human Pregnancy

Prostaglandin Production and Zinc Depletion in Human Pregnancy

The source of thromboxane and prostaglandins in experimental inflammation

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part I)

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