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At least 253 records · Page 14Linked to original sources
PubMed1985

Generation of C5a and prostacyclin (PGI2) in an inflammatory response to zymosan and a reversed passive Arthus-type reaction in the peritoneal cavity of the rabbit.

Exudate fluids were removed from the rabbit peritoneal cavity 2 h after the injection of zymosan or the initiation of a reversed passive Arthus-type reaction. Inflammatory oedema was measured using Evans blue dye extravasation and the concentrations of C5a and the PGI2 metabolite, 6-oxo-PGF1 alpha, were measured by radioimmunoassay. High levels of C5a were found in these inflammatory exudates and we suggest that the extravascular generation of C5a is important in the induction of increased microvascular permeability. The presence of PGI2 may have an enhancing effect on plasma protein leakage.

Animals↗
PubMed1983

Synthesis of complement by macrophages and modulation of their functions through complement activation.

During the last decade considerable progress has been made to characterize intimate functional links between macrophages, a major cellular component of immunoinflammatory responses, and the complement system representing the major humoral mediator of inflammation. Macrophages of various species and tissue sites have been shown to synthesize and release most of the complement components providing these cells with their own "pericellular" complement system. Circumstantial evidence for the assembly of both classical and alternative pathway convertases has been adduced. An intricate network of feedback loops involving endogenous and extrinsic factors operates to adjust complement production to acute requirements, for example augmenting production in the face of accelerated turnover at sites of inflammation, and returning it to baseline levels once the inflammatory stimulus has subsided, in order to maintain a fine-tuned balance. The molecular mechanisms underlying regulation of complement synthesis by macrophages are beginning to be elucidated by use of gene technology. On the other hand, complement activation products exert a number of effects on macrophages via specific surface receptors causing internalization of offending agents, microbes, and immune complexes, promotion of intracellular killing, controlling migration behavior, inducing release of potent biologic substances such as lysosomal enzymes, arachidonic acid metabolites, and interleukin 1. In these interactions, two important humoral mediator systems of inflammation, the complement system and the arachidonic acid cascade, are functionally linked at the level of the macrophage. Stimulation of the release of immunomodulating compounds from macrophages invoke a role for complement in immune regulation. This multifaceted interplay is of particular importance considering the mobility of macrophages that allows them to gain almost unrestricted access to sites of ongoing immunoinflammatory responses. The time seems to have come to abandon the petrified thinking in socalled systems as, for instance, humoral versus cellular, specific versus unspecific, and to proceed to interlocking functions guided by physiology proper.

Anaphylatoxins↗
PubMed1989

The effect of adherence on the generation of reactive oxygen species by human neutrophilic granulocytes.

Human neutrophilic granulocytes (PMN) suspended in protein containing salt solution or adherent on protein coated nylon fibers were tested for the production of H2O2 and O2- in response to various PMN stimulants. Upon stimulation with the chemotactic factors formyl-methionyl-leucyl-phenylalanine, C5a and platelet activating factor, the non-chemotactic ionophore A23187, and the chemotaxis inhibitors tumor necrosis factor (TNF alpha) and lymphotoxin (TNF beta) adherent PMN produced considerably more reactive oxygen metabolites than suspended cells. The relative amounts of the two metabolites varied with the stimulus and its concentration, TNF alpha and TNF beta favoring H2O2 production, C5a eliciting more O2- than H2O2 and the other active stimulants being in between. Leukotriene B4 and a novel monocyte-derived chemotaxin were inactive in releasing either oxygen derivative from adherent or suspended PMN. The data indicate that attachment of PMN to endothelial cells or to connective tissue substances can strongly enhance its ability to respond to a given stimulus with the production of reactive oxygen metabolites. The findings may in part explain the "priming" phenomenon since many PMN-priming mediators increase the cells' adherence.

Calcimycin↗
PubMed1988

Anaphylatoxin-induced release of histamine from in vitro perfused guinea pig kidney.

The effect of porcine C5a des Arg and C3a, given as a bolus injection, in the isolated constant flow pump-perfused guinea-pig kidney was investigated. Only C5a des Arg showed activity which was manifested by a dose-dependent increase in perfusion pressure (PP, due to vasoconstriction) and histamine release. Although histamine release was substantial, it alone could not account for the increase in PP. The two more likely causes are a direct vasoconstrictor effect and the release of other mediators.

Anaphylatoxins↗
PubMed1983

Vascular permeability changes induced by complement-derived peptides.

The polypeptides C3a and C5a are released as protein cleavage byproducts during activation of the complement system. These substances are able to release histamine from mast cells and this has generally been thought to be the link between complement activation and increased microvascular permeability in inflammatory reactions. Recent observations of inflammatory responses in the skin suggest that there is another link, which does not involve histamine. This is potentially of more general importance since antihistamines have limited effects on the majority of inflammatory reactions. One of the complement protein fragments, C5a (with or without carboxyl terminal arginine which is necessary for histamine release), is very potent in increasing vascular permeability. However, protein leakage leading to tissue oedema in skin is difficult to detect unless an arteriolar dilator is present. There is evidence that C5a and a vasodilator prostaglandin can be generated together extravascularly in response to a microbial stimulus. Unlike histamine, C5a does not act directly on venular endothelial cells, but triggers a very rapid interaction between circulating polymorphonuclear leukocytes and venular endothelial cells which, by an unknown mechanism, results in elevated venular permeability to plasma proteins.

Animals↗
PubMed1990

Measurement of complement activation products in patients with chronic rheumatic diseases.

Measurement of the complement activation products C1s:C1-inh, C3bP and C5b-9 by ELISA in plasma samples from normals, rheumatoid arthritis (RA) and systemic lupus erythematosis (SLE) patients showed significantly elevated levels in the two patient groups (P less than 0.0001 for C1s:C1-inh, C3bP and C5b-9) compared to normals. In seropositive RA patients there were significant correlations between the levels of the three complement activation complexes and IgM-RF, IgG-RF and IgA-RF. However, IgM-RF did not interfere with any of the ELISA systems. Mean levels of C1s:C1-inh, C3bP and C5b-9 were the same in paired plasma and synovial fluids; however, C3bP levels in the paired samples did not correlate with one another by rank. Our conclusions are that: (a) elevated plasma levels of these complement activation products are detectable in rheumatic diseases; (b) plasma levels of these complement activation products are related to Rheumatoid factor (RF) levels in seropositive RA patients; and (c) IgM-RF does not influence these solid-phase ELISA procedures.

Antibodies↗
PubMed1993

Membrane signaling by complement C5b-9, the membrane attack complex.

The terminal complement complexes C5b-7, C5b-8 and C5b-9 are able to generate nonlethal cell signals. One universal consequence of a cell being targeted by C5b-8 or C5b-9 is an influx of Ca2+. In addition, other second messengers, including cAMP, inositol phosphate intermediates and arachidonate metabolites, are generated by the terminal complement complexes in specific cell types. In vivo, terminal complement complexes have been found in a wide variety of inflammatory processes in humans and in experimental animal models. Some of these models of inflammation putatively induced by terminal complement complexes have been tested in complement-deficient animals, and indeed no inflammation results, which supports the critical role of the terminal complement complexes in the pathogenesis of the lesion.

Animals↗
PubMed1980

Chemotactic factor-induced membrane potential changes in rabbit neutrophils monitored by the fluorescent dye 3,3'-dipropylthiadicarbocyanine iodide.

Rabbit neutrophil leucocytes take up the cationic, fluorescent dye 3,3'-dipropylthiadicarbocyanine iodide (DiS-C3-(5)). Treatment with valinomycin and K+ then produces characteristic changes in suspension fluorescence that indicate that the dye enters the cells in a potential-dependent fashion and that the resting membrane potential lies between -66 and -86 mV. The peptide, N-fMet-Leu-Phe, a potent chemoattractant for neutrophils, added to stained cell suspensions, induces fluorescence intensity changes. These occur over an 8-10 min period. The time course of this response is profoundly affected by the omission of Ca2+ from the medium. When this ion is present (1.26 mM) a small, transient increase in intensity is observed, superimposed on a sustained decrease. On the other hand, in the absence of added Ca2+ a large, transient increase is observed. The ED50 for this is 1.1 x 10(-10) M. These changes are not elicited by N-fMet-Phe (10(-9) M) and are inhibited by the antagonist Boc-Leu-Phe-Leu-Phe. However, a component of zymosan-activated rabbit plasma, which is complement-derived, induces identical fluorescence changes that are not inhibited by the antagonist, confirming that neutrophil activation by complement operates through an independent receptor. The fluorescence responses to the chemotactic peptide and the activated-plasma component may be interpreted in terms of changes in neutrophil membrane potential brought about by alterations in cell ionic permeability at an early stage during activation. The transient increase corresponds to a depolarisation that may be associated with a change in Na+ permeability, while the sustained decrease corresponds to a membrane hyperpolarisation.

Anaphylatoxins↗
PubMed1983

Direct demonstration of increased intracellular concentration of free calcium in rabbit and human neutrophils following stimulation by chemotactic factor.

An increase in the level of intracellular free calcium concentration in rabbit and human neutrophils stimulated by chemotactic factors has been demonstrated directly using the calcium-sensitive fluorescent probe quin-2. Addition of f-Met-Leu-Phe (10(-9) M), C5a (3 x 10(-9) M) or leukotriene B4 (6 x 10(-8) M) to the neutrophils induces a rapid increase in the intracellular concentration of free calcium that reaches a maximum value 15 seconds following stimulation. At concentrations of f-Met-Leu-Phe less than 10(-8) M the enhancement is dose dependent with an ED50 of 8 x 10(-11) M and is significantly reduced in the presence of EGTA in the suspending medium.

Aminoquinolines↗