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Results for “Complement C5”

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At least 1,621 records · Page 90Linked to original sources
PubMed1988

Transendothelial chemotaxis in vitro of human monocytes.

Porcine aortic vascular endothelial cells were grown to confluence on microporous PTFE membranes and incorporated into a two-compartment chemotaxis assembly. Human peripheral blood mononuclear cells (20-25% monocytes) were placed in the upper compartment and zymosan-activated human serum (ZAHS) as chemoattractant in the lower compartment. Over a 3 h period monocytes migrated across the endothelialized membrane and adhered to a collecting filter sited in the lower compartment. Addition of ZAHS to the cell suspension in the upper compartment virtually abolished the migration response whilst only minimal leucocyte migration was supported by the bare unendothelialized PTFE membrane. The extent of transendothelial monocyte chemotaxis was dependent upon the concentration of chemoattractant in the lower compartment and upon the cell density of the suspension containing monocytes. A confluency test of fluid flow across the endothelialized filter showed that monocyte migration could take place without disturbing endothelial barrier function. The culture system is easy to assemble and the method provides experimental versatility.

Animals↗
PubMed1985

Pharmacological investigation of the mechanisms of platelet-activating factor induced mortality in the mouse.

Although the platelets of the mouse are refractory to the direct effects of platelet-activating-factor (PAF), tail vein injection of 10-150 micrograms/kg PAF produces lethal anaphylactic shock. Sensitivity varies with strain and source: Swiss Webster mice show a range of sensitivity and DBA/2 (complement C5-deficient) mice are very resistant. At lethal doses of PAF, animals show labored respiration and general depression; death occurs within 15-45 min. Dexamethasone administered at least 1.5 hr prior consistently protects, whereas the cyclooxygenase inhibitors do not. Antihistamines, adrenergic antagonists, and methysergide have no effect, but cyproheptadine is partially protective at near lethal doses. Calcium entry blockers and calcium chelators, tetracycline and chlortetracycline are partially protective at very high doses consistent with non-specific effects on calcium dependent processes. The arachidonic acid lipoxygenase inhibitors BW755c, phenidone, nordihydroguaiaretic acid and diphenyldisulfide provide nearly complete protection after oral administration of 50-200 mg/kg. Phosphodiesterase inhibitors and dapsone are also effective orally. The leukotriene antagonist FPL55712 administered intraperitoneally (10 mg/kg) 5 min. prior to PAF challenge provides almost complete protection. PAF-induced mortality in the mouse represents a small animal model of systemic anaphylaxis particularly useful for the systemic testing of arachidonic acid lipoxygenase inhibitors and leukotriene antagonists.

Anaphylaxis↗
PubMed1977

Complement-mediated release of histamine from human basophils. III. Possible regulatory role of microtubules and microfilaments.

The release of histamine by normal human leukocytes (basophils) following in vitro challenge with activated complement (zymosan-treated serum) was previously reported. In this study, the effects of various pharmacologic agents on this release mechanism were compared with allergen-induced release of histamine. Colchicine and vinblastine antagonize the polymerization of tubulin to form microtubules, and both agents inhibited complement-and allergen-triggered release of histamine from basophils. Finally, treatment with cytochalasin B, a fungal product known to interfere with microfilament formatin, resulted in enhanced release of histamine from complement-treated basophils but no significant change in the percentage of histamine released from allergen-treated basophils. These findings suggest that microtubules and/or microfilaments are involved in complement-induced secretion of histamine by human basophils.

Allergens↗
PubMed1980

Chemotaxis.

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Animals↗
PubMed1985

Chemotaxis of macrophage in inflammation.

Our particular attention in this article was given to natural mediators for macrophages isolated from the sites of tissue injury. A number of chemotactic factors, which may satisfy many criteria making them acceptable as inflammatory leucocyte chemotactic factors, has been separated. Among them, our laboratory has isolated three macrophage (monocyte) chemotactic factors (MCF-a, -b and -c). Their purification, characterization and functional specificity are discussed.

Animals↗
PubMed1980

Size increase induced in Walker ascites cells by chemotactic factors.

Upon interaction with the tumor cell chemotactic factor derived from zymosan-activated serum or with the synthetic chemotactic factor, formylmethionyl-leucyl-phenylalanine (f-met-leu-phe), the number of Walker 256 carcinosarcoma cells in suspension dropped as measured by a Coulter Counter. The drop in the number of cells counted by the Coulter Counter was accompanied by and possibly attributed to a swelling in the mean cell volume of approx. 20%. These effects were blocked by the addition of 2-deoxy-d-glucose, along with the chemotactic factors, to the tumor cells. The doses of the chemotactic factors which induced these responses paralleled closely the doses which have been shown to induce a chemotactic response as measured in the Boyden Chamber assay. These findings indicate that non-leukocytic cells, like leukocytes, are capable of other responses in addition to chemotactic migration in the Boyden chamber assay upon interaction with appropriate chemotactic factors.

Animals↗
PubMed1992

Comparative mapping of mouse chromosome 2 and human chromosome 9q: the genes for gelsolin and dopamine beta-hydroxylase map to mouse chromosome 2.

The mapping of human chromosome 9 (HSA9) and mouse chromosome 2 (MMU2) has revealed a conserved syntenic region between the distal end of the long arm of chromosome 9 and proximal mouse chromosome 2. Two genes that map to human chromosome 9q34, gelsolin (GSN) and dopamine beta-hydroxylase (DBH), have not previously been located in the mouse. We have used an interspecific backcross to map each of these genes, by Southern blot analysis, to mouse chromosome 2. Gelsolin (Gsn) is tightly linked to the gene for complement component C5 (Hc), and dopamine beta-hydroxylase (Dbh) is just proximal to the Abelson leukemia virus oncogene (Abl) and alpha-spectrin 2 (Spna-2). The loci for gelsolin and dopamine beta-hydroxylase therefore form part of the conserved synteny between HSA9q and MMU2.

Animals↗
PubMed1995

Oxidation of methionyl residues in proteins: tools, targets, and reversal.

Methionine (Met) is one of the most readily oxidized amino acid constituents of proteins. It is attacked by H2O2, hydroxyl radicals, hypochlorite, chloramines, and peroxynitrite, all these oxidants being produced in biological systems. The oxidation product, Met sulfoxide, can be reduced back to Met by Met sulfoxide reductase. Numerous proteins lose functional activity by Met oxidation. However, functional activation of proteins by Met oxidation has also been observed. Functional changes by Met oxidation in a given protein appear to have pathophysiological significance in some cases. Considering the reversibility of Met oxidation and the functional changes associated with the oxidation, it seems possible that Met oxidation/reduction in proteins may be one means to control homeostasis in biological systems.

Complement C5↗