Complement and the Mononuclear Phagocyte System

Lappin, David F.; Whaley, K

doi:10.1007/978-1-4757-9534-9_4

Cited by 3 publications

(2 citation statements)

References 171 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…At present, little is known of the effects of glucocorticoids on the biosynthesis of complement components. In earlier studies it was observed that glucocorticoids stimulated synthesis of the second component of complement (C2), factor B (B) and Cl inhibitor (Cl-inh) (McPhaden et al, 1982;Lappin & Whaley, 1989), and their effects on human umbilical vein endothelial cells were to increase factor H synthesis and decrease C3 and B synthesis (Dauchel et al, 1990). However, the mode of action of these agents was not investigated.…”

Section: Introductionmentioning

confidence: 99%

Modulation of complement gene expression by glucocorticoids

Lappin

Whaley

1991

Biochemical Journal

View full text Add to dashboard Cite

The addition of dexamethasone, prednisolone or cortisol (in order of efficacy) to human monocytes in culture produced dose-related increases in the synthesis rates of the complement components C1 inhibitor (C1-inh), factor B (B) and C2. In contrast, concentrations of C3 and lysozyme in the culture supernatants were decreased. Indomethacin stimulated synthesis of C1-inh, C2 and B, but had little effect on synthesis of C3 or lysozyme. The simultaneous addition of cycloheximide (2.5 micrograms/ml) abrogated the effects of dexamethasone on synthesis of C2, B and C1-inh, but the effect of indomethacin on the synthesis of these components was unchanged. These data suggest that protein synthesis is required for the effects of glucocorticoids on the synthesis of C2, B and C1-inh to occur. Dexamethasone and indomethacin increased the abundances of C1-inh mRNA, B mRNA and C2 mRNA in parallel with changes in the synthesis rates of these proteins. The changes in mRNA abundance were not transcriptional, but were shown to be due to increased mRNA stability. In contrast, dexamethasone decreased the expression of C3 and lysozyme by decreasing the rate of transcription of these genes. Indomethacin had no effect on transcription of the C3 and lysozyme genes. The half-lives of C3 mRNA, lysozyme mRNA and actin mRNA were not altered by dexamethasone or indomethacin. It is concluded that the effects of glucocorticoids on monocyte synthesis of C2, B and C1-inh are due to increased mRNA stability and may be related to inhibition of prostaglandin synthesis, as these effects are similar to those produced by indomethacin. The effects of dexamethasone on the synthesis of C3 and lysozyme differ from those on C2, B and C1-inh as they depend upon a decrease in gene transcription, which is not affected by indomethacin.

show abstract

Section: Introductionmentioning

confidence: 99%

Modulation of complement gene expression by glucocorticoids

Lappin

Whaley

1991

Biochemical Journal

View full text Add to dashboard Cite

show abstract

“…Of particular importance is the presence of complement in the infected skin. Complement has been shown to possess a devastating effect on gyrodactylids (Harris et al 1997, Buchmann 1998 and is known to be produced by macrophages at least in mammals (Lappin & Whaley 1993). As gyrodactylids are seen to escape surface areas rich in mucous cells and macrophages during the response phase (Buchmann 1997, Buchmann & Bresciani 1998, Lindenstrnn & Buchmann 1998, it could be suggested that macrophages in the skin have some influence on the amount of complement and mucous cells in the fish skin and thereby affect the microenvironment of these ectoparasites.…”

Section: Introductionmentioning

confidence: 99%

Rainbow trout leucocyte activity:influence on the ectoparasitic monogenean Gyrodactylus derjavini

Buchmann¹,

Bresciani²

1999

Dis. Aquat. Org.

View full text Add to dashboard Cite

The ectoparasitic monogenean Gyrodactylus deqavinl from ralnbow trout Oncorhynchus mykiss was exposed in vltro to macrophages isolated as pentoneal exudate cells or as pronephros cells from the host Cells colonized the parasite especially in the mannose-nch regions in the c e p h a l~c ducts where ciliated structures were abundant Opsonizatlon wlth fresh serum, in contrast to heatinactivated serum, enhanced colonlzat~on also on other body parts The adverse effect of the activated macrophages towards G derjavlnl was assoc~ated with a heat-lab~le component released from these cells to the culture medium Analysis of substances released from the cells showed leactivity for a number of enzymes, complement factor C3, ~nterleukin (11-1) and reactive oxygen metabohtes Chemotaxls assays with pronephnc leucocytes showed chemoattractants in G derlavini and the respiratory burst level of macrophages was slightly elevated due to parasite exposure It is suggested that skln leucocytes contribute to an increased level of complement factors in the trout skln during the host response, whereby a hostlle m~croenvironment for the parasites IS created In addition, the 1L-l production could affect mucous cell secretion and hyperplasia and add to the antiparasitlc actlon of the epithelium Likewise react~ve oxygen metabolites and vanous enzymes are l~k e l y to be involved In the skin response

show abstract

Lead disrupts eicosanoid metabolism, macrophage function, and disease resistance in birds

Knowles

Donaldson

1997

Biol Trace Elem Res

View full text Add to dashboard Cite

Lead (Pb) affects elements of humoral and cell-mediated immunity, and diminishes host resistance to infectious disease. Evidence is presented supporting a hypothesis of Pb-induced immunosuppression stemming from altered fatty acid metabolism, and mediated by eicosanoids and macrophages (MO). Chronic Pb exposure increases the proportion of arachidonate (ArA) among fatty acids in lipid from avian tissues, and this change provides precursors for eicosanoids, the oxygenated derivatives of ArA that mediate MO acute inflammatory response. In the current study, we showed that the concentration of ArA in phospholipids of MO elicited from turkey poults fed 100 ppm dietary Pb acetate was twice that of controls. In vitro production of eicosanoids by these MO was substantially increased, and this effect was most pronounced following lipopolysaccharide stimulation: prostaglandin F2 alpha was increased 11-fold, thromboxane B2 increased threefold, and prostaglandin E2 increased by 1.5 times. In vitro phagocytic potential of these MO was suppressed, such that the percentage of MO engulfing sheep red blood cell (RBC) targets was reduced to half that of control MO. In vivo susceptibility of Pb-treated and control birds to Gram-negative bacteria challenge was also evaluated. The morbidity of chicks inoculated with Salmonella gallinarum and fed either control or 200 ppm Pb acetate-supplemented diets was similar, except early in the course of the disease when mortality among Pb-treated birds was marginally greater. In these studies, effects of Pb that could influence immunological homeostasis were demonstrated for MO metabolism of ArA, for production of eicosanoids, and for phagocytosis. There was also the suggestion that these in vitro indices of immune function are related to in vivo disease resistance.

show abstract

Complement and the Mononuclear Phagocyte System

Cited by 3 publications

References 171 publications

Modulation of complement gene expression by glucocorticoids

Modulation of complement gene expression by glucocorticoids

Rainbow trout leucocyte activity:influence on the ectoparasitic monogenean Gyrodactylus derjavini

Lead disrupts eicosanoid metabolism, macrophage function, and disease resistance in birds

Contact Info

Product

Resources

About