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At least 433 records · Page 24Linked to original sources
PubMed1983

5-L-hydroxy-6,8,11,14-eicosatetraenoate potentiates the human neutrophil degranulating action of platelet-activating factor.

Platelet-activating factor (AAGPC) and two of its structural analogues degranulated human neutrophils with respective potencies that were increased up to 100 to 1000-fold by 16 nM to 5 microM of 5-L-hydroxyeicosatetraenoate (5-L-HETE). 5-rac-HETE had similar actions but 8-rac-HETE was without effect. Furthermore, 5-L-HETE did not influence the degranulating actions of C5a, A23187 or a formalated oligopeptide chemotactic factor and none of the HETEs, by themselves, caused degranulation. Thus, 5-L-HETE and AAGPC selectively interact to induce degranulation. Since these products rapidly form in stimulated PMNs, they may serve as potentiator and agonist, respectively, to transduce biological signals into cell function.

Arachidonic Acids↗
PubMed1987

Lack of correlation between calcium mobilization and respiratory burst activation induced by chemotactic factors in rabbit polymorphonuclear leukocytes.

Low concentrations of FMLP, partially purified rabbit C5a, leukotriene B4 and platelet activating factor induced a rapid rise of intracellular free Ca2+ in rabbit polymorphonuclear leukocytes. However, the four factors differed markedly in their ability to activate the respiratory burst. The peptides FMLP and C5a induced a single, strong chemiluminescence response whereas the lipids leukotriene B4 and platelet activating factor induced a markedly less intense response with a two-peak profile. Respiratory burst activation by the peptides was dependent on extracellular Ca2+ whereas the lipids required both Mg2+ and Ca2+. The results indicate that mobilization of intracellular Ca2+ is insufficient by itself to induce respiratory burst activation and that the intracellular pathways leading to activation differ depending on the nature of the stimulus.

Animals↗
PubMed1987

Oscillatory motion in human neutrophils responding to chemotactic stimuli.

Human neutrophils treated with the secretion inhibitor 17-hydroxywortmannin were stimulated with fMLP, C5a, PAF or LTB4, and the ensuing shape change was studied. The cells rapidly extended lamellipodia and showed regular oscillatory behaviour. The oscillations were observed in both light transmission and 90 degrees light scattering, had the same frequency in each case, and disappeared within 30-50 seconds. Light scattering theory suggests that they reflect rhythmic changes in the shape and/or size of the chemotactically stimulated cells, possibly related to crawling or swimming movements associated with migration.

Androstadienes↗
PubMed1987

Synthesis of a new photoreactive C5a analog that permits identification of the ligand binding component of the granulocyte C5a receptor.

Human C5a is a complement derived inflammatory mediator that binds to specific receptors that are found in the granulocyte plasma membrane. A new photoreactive C5a analog, that can be radiolabeled in the aryl azide moiety, has been synthesized by coupling p-azidosalicyl-2-mercapto-N-ethylamide-2'-thiopyridine disulfide to a partially reduced form of C5a. This unique analog (ASAMEA-SC5a) specifically bound to the granulocyte C5a receptor with an apparent Kd of 1.8 nM, a value that is comparable to that of the native ligand. Photoactivation resulted in crosslinking of this probe to the granulocyte C5a receptor. Subsequent reductions of the complex produced a radiolabeled C5a receptor, or a subunit of this receptor that had an apparent molecular weight of 47,000 Daltons on SDS-PAGE.

Affinity Labels↗
PubMed1987

Activation of human serum complement with allergens. I. Generation of C3a, C4a, and C5a and induction of human neutrophil aggregation.

To understand the relevance of allergens in generation of C3a, C4a, and C5a in normal human serum, we studied extracts of several allergens (house dust, house dust mite, Aspergillus fumigatus, and perennial ryegrass). Known complement activators zymosan and endotoxin were used as controls. Generation of C3a, C4a, and C5a (determined by radioimmunoassays) occurred with extracts of house dust and Aspergillus more than with house dust mite and ryegrass. Anaphylatoxins were produced both in dose and time-dependent fashions. Serum activated with house dust and Aspergillus extracts induced neutrophil aggregation when this serum was added to neutrophil suspensions. Less aggregation occurred when house dust mite and perennial ryegrass extract-activated sera were added to human neutrophils. We propose that some allergens may induce biologic responses by activation of sera and generation of anaphylatoxins as well as by IgE-mediated responses.

Adult↗
PubMed1984

Severe pulmonary hypersensitivity associated with passive transfusion of a neutrophil-specific antibody.

A life-threatening pulmonary hypersensitivity reaction accompanied by profound leucopenia and transient hypocomplementaemia developed in a 73-year-old man after repair of an abdominal aortic aneurysm. A neutrophil-specific antibody, anti-NA2) was demonstrated by granulocyte immunofluorescence and microagglutination in one of the transfused donor units. In addition, activated complement component C5a was generated in vitro by incubation of the patient's serum with the aortic graft material. This severe clinical reaction may have resulted from the interaction of the transfused anti-NA2 antibody with complement activation induced by the aortic graft material.

Aged↗
PubMed1985

Anaphylatoxin C5a modulation of an alpha-adrenergic receptor system in the rat hypothalamus.

C5a anaphylatoxin injected via implanted cannulae into the perifornical region of the hypothalamus stimulated eating in sated rats. C5a also attenuated carbamyl choline-induced drinking, and carbamyl choline inhibited C5a-induced eating, a mutual inhibition characteristic of the adrenergic-cholinergic interactions at this site. The increased food intake induced by C5a was also reversed by phentolamine, an alpha-adrenergic antagonist. Granulocytes infiltrating as a result of C5a-mediated leukotaxis did not arrive at the site in time to influence C5a activity. We propose that C5a in some way activates an alpha-adrenergic receptor system in the hypothalamus, and that anaphylatoxins could mediate neuropsychiatric symptoms sometimes associated with immune complex diseases affecting the central nervous system.

Animals↗
PubMed1983

Role of filter-bound IgA in inhibiting polymorphonuclear leukocyte chemotaxis.

The effects of human serum IgA on human polymorphonuclear leukocyte (PMN) function were studied. In Boyden chambers, chemotactic migration against semipurified C5a as well as the formylated tripeptide FMLP was inhibited in the presence of IgA. Under such conditions, the release of superoxide anion was not changed. In addition, chemotaxis "under agarose" using the leading front evaluation remained unaltered in the presence of IgA despite IgA-induced aggregation of PMN and reduced density of migrating cells. Chemotaxis filters incubated with radiolabelled IgA demonstrated strong binding of IgA, and further, these IgA-pretreated filters impeded PMN migration. Incubation of PMN with IgA followed by subsequent washings did not affect chemotactic migration. These data show that filter binding of IgA is responsible for the inhibition of chemotactic PMN-migration in the Boyden chambers, most probably mediated by increased cell-substrate adhesion. Experiments using casein showed displacement of IgA by casein which enables PMN to fully respond to casein.

Binding Sites, Antibody↗
PubMed1985

Influence of antibody and complement components on phagocytosis and chemiluminescence of macrophages.

Macrophages are known to release reactive oxygen species (O2-, 1O2, H2O2, OH.) in response to various membrane stimuli. However, our studies show that phagocytic stimulation of macrophages is not necessarily accompanied by a stimulation of the oxidative burst. Whereas IgG-opsonized erythrocytes were capable to induce phagocytosis and a chemiluminescence response, both being dependent on the number of IgG bound per erythrocyte, C3b-bearing erythrocytes were well ingested but failed to induce any chemiluminescence reaction. Furthermore, stimulation of macrophages, via the Fc-receptors, seems to alter their functional state in regard to the activation of a receptor, which enables them to recognize membrane lesions on the target erythrocyte. The presence of IgG and membrane lesions, e.g. the C5b-9-complex of complement, induced a marked increase in chemiluminescence compared with stimulation by IgG-bearing particles alone. The augmented response of macrophages was at least in part due to an additional release of H2O2, which was not liberated in response to IgG-bearing erythrocytes. This "lesion recognizing receptor" in the macrophage membrane could not be activated by stimulation of C3b-receptors, indicating its functional linkage to the Fc-receptors.

Animals↗
PubMed1987

Differences between membranoproliferative glomerulonephritis types I and III in clinical presentation, glomerular morphology, and complement perturbation.

Data for 26 patients with membranoproliferative glomerulonephritis, type I (MPGN I) and 22 with membranoproliferative glomerulonephritis, type III (MPGN III), as distinguished by glomerular ultrastructure, were analyzed to determine differences in presentation, complement perturbation, and glomerular morphology by light microscopy. MPGN III was detected with greater frequency by the chance discovery of hematuria and proteinuria in the otherwise healthy individual (MPGN III, 63%; MPGN I, 30%; P = .01) and never, in the absence of renal failure, presented with systemic symptoms such as ease of fatigue, weight loss, and pallor, as may patients with MPGN I. The more frequent detection of MPGN III by chance is evidence that its onset is insidious and that for long periods it produces no symptoms or signs. Glomerular proliferation is also less than in MPGN I. Further, in MPGN III, the complement perturbation and glomerular immunofluorescence give no evidence of classical pathway activation, for which there is abundant evidence in MPGN I. Even with severe hypocomplementemia in MPGN III, C3 nephritic factor, another cause of hypocomplementemia, is rarely detectable and then in very low concentration. The cause of the complement perturbation in MPGN III has so far escaped identification. Although these observations give evidence that MPGN III is distinct from MPGN I, there is compelling evidence from other studies that a predisposition to both types is inherited and that similar genetic factors are operative in the two types. Because their genetic basis appears to be the same, it must be concluded that despite their differences, types I and III are variants of the same disease.

Complement C3↗