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At least 991 records · Page 55Linked to original sources
PubMed2002

Soluble complement receptor type 1 protects rats from lethal shock induced by anti-Crry antibody following lipopolysaccharide priming.

BACKGROUND: In rats primed with a trace amount of lipopolysaccharide (LPS), acute lethal shock is induced following the injection of monoclonal antibody against a membrane inhibitor of complement (anti-Crry). Administration of cobra venom factor to exhaust complement before the LPS priming can prevent the lethal reaction. Therefore, we evaluated whether soluble complement receptor type 1 (sCR1), which inhibits complement reaction, can interfere with lethal shock when administered after LPS priming or even after anti-Crry injection. METHODS: sCR1 was administered intravenously before or after the administration of anti-Crry, and the effects on blood pressure and acute lethality were determined. RESULTS: Administration of sCR1 could rescue rats from lethal shock even when it was administered after anti-Crry injection, which immediately causes a blood pressure decrease leading to lethal shock. CONCLUSION: sCR1 may be an effective treatment for acute shock involving complement activation.

Animals↗
PubMed2004

Membrane complement regulatory proteins in autoimmune and inflammatory tissue injury.

The complement system plays a complex role in the pathogenesis of autoimmune diseases. It inhibits autoimmunity development by helping to maintain self-tolerance and/or by facilitating the disposal of immune complexes and apoptotic cell antigens. On the other hand, complement activation is thought to contribute significantly to end organ damage in antibody-mediated autoimmune and inflammatory conditions, although the relevant importance of complement and Fe receptor pathways in these processes has recently been debated. To avoid autologous complement-mediated tissue injury, host cells normally express a number of soluble and membrane-bound complement regulatory proteins. Recent studies with gene knockout mice have suggested that membrane-bound complement regulatory proteins may critically determine the sensitivity of host tissues to complement injury in autoimmune and inflammatory disorders. Evidence is also accumulating to support the hypothesis that membrane complement regulatory proteins may not only inhibit complement-mediated injury during the effector phase of autoimmunity but also influence the adaptive immune response through complement-dependent or -independent mechanisms. The latter mechanism is likely related to their potential as cell surface signaling molecules.

Animals↗
PubMed2004

Analysis of the optimal blood sampling conditions for estimation of hematopoietic progenitor cell count by the SE-9000 automated hematolyzer.

We evaluated the optimal conditions for blood sampling for hematopoietic progenitor cells (HPCs) as estimated by the immature information program of the SE-9000 automated hematology analyzer. The HPC count was most stable when the blood samples were incubated at room temperature with ethylene-diaminetetraacetic acid dipotassium (EDTA-2K) as an anticoagulant. The HPC count should, however, be measured within 4 h after blood collection, even under optimal conditions. In contrast, the CD34+ cell count estimated by flow cytometric analysis was stable for at least 21 h after the blood samples were incubated with EDTA-2K at room temperature or 4 degrees C. When appropriate blood samples were used, the HPC count in the peripheral blood significantly correlated with the CD34+ cell count in the peripheral blood and in the apheresis yields (r = 0.798 and 0.635, respectively); therefore, the HPC count is a reliable predictor for initiation of apheresis procedures to obtain sufficient HPCs for peripheral blood stem cell transplantation.

Adolescent↗
PubMedDate not supplied

Up-regulation of cytoskeletal proteins in activated microglia.

OBJECTIVES: This study investigates how the tumor necrosis factor (TNF-alpha) and interleukin-1beta (IL-1beta) affect the morphology, organization, and expression of actin, beta-actin and tubulin in microglia. MATERIALS AND METHODS: Microglia cultures were prepared from neopallia of newborn mice. Immunofluorescence, immunoblotting, and ELISA studies were used. RESULTS: When microglia are treated with TNF-alpha, IL-1beta or a combination of both for 1-5 days, the majority change from an ameboid to a large, round and flat shape. F-actin and beta-actin isoform, which are diffusely arranged throughout the cytoplasm before stimulation, are reorganized into filamentous bundles underneath and parallel to the cell membrane, which projects into many ruffles. This organization is maintained even after withdrawal of the cytokines. The dense microtubule network of tubulin in nontreated microglia becomes less dense and extends to occupy the cytoplasm of the treated microglia. Immunoblotting shows that the amount of total actin, beta-actin isoform and tubulin increases in treated microglia. In addition, IL-1beta and a combination of both TNF-alpha and IL-1beta stimulate the release of IL-6 by microglia. CONCLUSION: This study suggests that TNF-alpha and IL-1beta have an effect on the expression of cytoskeletal proteins similar to some extent to that of LPS. The up-regulation of actin, beta-actin and tubulin may play a key role in the motility and recruitment of microglia to the area of central nervous system inflammation.

Actins↗
PubMed2005

Band 3/complement-mediated recognition and removal of normally senescent and pathological human erythrocytes.

Band 3 modifications that normally occur during physiological red blood cell (RBC) senescence in humans, and occasionally in pathological conditions are described in the context of their role in enhancing RBC recognition and phagocytic removal. Band 3 modifications are mostly due to oxidative insults that gradually accumulate during the RBC lifespan or impact massively in a shorter time period in pathological conditions. The oxidative insults that impact on the RBC, the protective mechanisms that counteract those damages and the phenotypic modifications that accumulate during the RBC lifespan are described. It is shown how specific oxidative as well as non-oxidative band 3 modifications enhance RBC membrane affinity for normally circulating anti-band 3 antibodies, and how membrane-bound anti-band 3 antibodies bring about a limited complement activation and membrane deposition of complement C3 fragments. The partially covalent complexes between anti-band 3 antibodies and complement C3 fragments are very powerful opsonins readily recognized by the CR1 complement receptor on the phagocyte. Band 3 modifications typically encountered in old RBCs have crystallized to a number of band 3-centered models of RBC senescence. One of those band 3-centered models, the so-called 'band 3/complement RBC removal model' first put up by Lutz et al. is discussed in more detail. Finally, it is shown how the genetic deficiency of glucose-6-phosphate dehydrogenase (G6PD) plus fava bean consumption, and a widespread RBC parasitic disease, P. falciparum malaria, may lead to massive and rapid destruction of RBCs by a mechanism comparable to a dramatic, time-compressed enhancement of normal RBC senescence.

Anion Exchange Protein 1, Erythrocyte↗
PubMed1991

Monocyte phenotype and interleukin-1 production in patients undergoing haemodialysis.

The expression of MHC class II (HLA-DR) and complement receptor (CR1) surface molecules on CD 14+ monocytes were compared with the production of the monokine interleukin-1 beta (IL-1 beta) in patients with endstage renal disease undergoing maintenance haemodialysis (HD) with hollow fibre dialyzers containing cellulose (CE, n = 8) and polysulfone (PS, n = 7) membranes. Monocyte staining was performed in blood samples obtained at the beginning and after 3 h of HD. Analysis of surface marker expression was done by immunofluorescence staining and flow cytometry analysis. Specific fluorescence intensity for both CR1 and class II (HLA-DR) antigens was increased in patients treated with CE membranes at the beginning of a dialysis treatment when compared to healthy control values. Interestingly, after 3 h on dialysis a further increase was noted for CR1 complement receptor expression whereas the increased HLA-DR expression was no longer detectable. In contrast, specific fluorescence intensity for both antigens was not significantly different from controls, either before or after dialysis, in patients treated with PS. The capacity of peripheral blood mononuclear cells to produce IL-1 beta spontaneously in vitro in the two patient groups was found to parallel results on phenotypic expression of surface molecules. The present study demonstrates that functional signs of monocyte activation, as evidenced by an augmented IL-1 beta production, in some patients on long-term HD correlate with an increased expression of two functionally important monocyte surface marker molecules.

Adult↗
PubMed1995

Another function of erythrocytes: transport of circulating immune complexes.

OBJECTIVE: To review the main characteristics of the 'immune complex (IC) transport system of erythrocytes', and its possible relevance for transfusion medicine. DATA SOURCES: Literature search, and results Of Studies performed in the laboratory of Dr J. Schifferli from 1986 to 1995. SELECTION CRITERIA: Peer review journals and work relevant to the topic. RESULTS: When antigen/antibody IC form in the presence of complement. C3b binds covalently to the complexes. Such opsonized complexes attach to cells bearing complement receptor 1 (CR1), which is mostly found on erythrocytes in the circulation. This allows IC to be transported through the circulation to the fixed macrophage system of the liver and spleen. In addition, C3b bound to the complexes is catabolized by factor 1 (with CR1 as a cofactor) so that the complement-activating properties of the complexes are reduced. CONCLUSIONS: Complement and erythrocyte CR1 contribute to the safe and effective elimination of IC in humans. This physiologic system prevents IC deposition in the vessel walls.

Antigen-Antibody Complex↗
PubMed1983

A simple solid phase radioimmunoassay specific for human C3b to detect C3b receptors on human lymphoblastoid cell surfaces.

Our aim was to detect C3b receptors on human lymphoblastoid cells using a solid phase radioimmunoassay (RIA) specific for human C3b. RIA was performed by coupling rabbit antihuman C3b to acrylamide beads to make immunobeads. The specificity and sensitivity of binding of 125I-C3b to immunobeads allowed the detection of as little as 6 X 10(-10) M unlabeled human C3b. The cells were incubated with a C3b concentration (10(-9) M) giving 25% inhibition in the RIA. The concentration of unbound C3b was then measured in the cell supernatants using RIA. Results showed that: (a) loss of C3b antigen in the cell supernatant was not due to degradation of C3b molecules, (b) C3b binding could be detected at 37 degrees C on the four B cell lines, but not on the two T cell lines or on the two non T-non B cell lines tested, (c) C3b bound on the B lymphoblastoid cells was not cleaved, neither into iC3b nor C3c and C3d fragments, supporting the presence of C3b receptors on the cells tested. This method allows screening of a variety of C3b receptor-positive cells.

Animals↗
PubMed1985

New developments in immunopathology with special reference to complement and immune complexes.

The last few years have seen rapid advances in our understanding of immune phenomena, and these are now being translated into a new understanding of immunopathology. This paper reviews a number of areas where important new knowledge has been gained in the area of complement and immune complexes as a cause of disease. An understanding of the role of the metabolism of complement proteins has led to an understanding of how these proteins interact with receptors to cause phagocytosis. New understanding of the lysis-producing steps has led to new diagnostic tests for complement-induced damage as well as new knowledge of how complement functions to kill microorganisms. New methods for purifying anaphylatoxins have made these proteins available for study in man. A model of serum sickness in man has allowed for the more detailed understanding of how immune complexes cause disease and has led to the appreciation of new clinical signs of immune-complex-mediated disease in man.

Antigen-Antibody Complex↗
PubMed1988

Erythrocyte CR1 receptors in patients with hypogammaglobulinaemia.

Erythrocyte CR1 receptors were measured in 16 patients with primary hypogammaglobulinaemia and compared with those in 14 normal controls. There was no significant difference in the number of receptors in the two populations. One patient with hypogammaglobulinaemia had a very low number of receptors and subsequently developed red cell aplasia.

Agammaglobulinemia↗
PubMed1990

Glomerular CR1 express in situ cofactor activity for degradation of C3b.

Adherence of sheep erythrocytes (E) sensitized with IgM antibodies (A) and C3b (EAC3b) to C3b/C4b receptors (CR1) in cryostat sections of human renal glomeruli was studied using the closed chamber technique. The adsorption was stable for at least 3 h at 37 degrees C. In the presence of purified factor I, the indicator cells, however, detached from the sections after 30 min at 37 degrees C. Factor H was not required. The release was not due to loss of CR1 activity in the tissue. The detached indicator cells were negative in the immune adherence test and were agglutinated by antibody to C3d, but not by antibody to C3c. Western blot of the detached indicator cells revealed the presence of C3d and C3c was found in the chamber fluid. Accordingly, detachment of the indicator cells was due to degradation of C3b to C3d with the release of C3c into the chamber fluid. Protease inhibitors did not prevent the detachment of the indicator cells. EAC3b incubated with sections of renal glomeruli preincubated with anti-CR1 antibody were not degraded. The results therefore indicate that CR1 in situ in renal glomeruli can provide the necessary cofactor activity for factor I-mediated degradation of C3b to C3d and C3c.

Complement C3b↗
PubMed1991

Effects of corticosteroids on cytokine generation and expression of activation antigens by monocytes in bronchial asthma.

The capacity of corticosteroids to inhibit the secretion of cytokines and the expression of selective antigens on monocytes has been studied in corticosteroid-sensitive (CS) and corticosteroid-resistant (CR) asthmatic patients. Incubation of monocytes derived from CS subjects with hydrocortisone inhibited the production of the enhancing activity, whereas in CR subjects hydrocortisone at concentrations of up to 10(-4) M did not suppress the release of enhancing activity. There was a rank order of potency for corticosteroid action: hydrocortisone less than methylprednisolone less than dexamethasone. The major activity was characterized as a heat-sensitive peptide of 3,000 daltons. The expression of CR1, CR3 and class II on asthmatic peripheral-blood mononuclear cells was increased relative to normal control donors. Culturing monocytes for 24 h in the presence of 10(-4) M hydrocortisone inhibited the expression of CR1, CR3 and class II in CS subjects but not in CR individuals. These results suggest that monocytes of CR asthmatic patients can increase the inflammatory potential of neutrophils and that they are hyperactive, as indicated by increased cytokine production and enhanced expression of activation markers, despite the presence of corticosteroids.

Adrenal Cortex Hormones↗
PubMed1996

Expression of complement regulatory proteins on fetal blood cells in utero.

Since the fetus is semiallogenic to the mother, mechanisms have evolved to protect fetal tissue from the maternal immune response. Among these mechanisms is the expression of cell-surface complement regulatory proteins at the maternal-fetal interface. However, beginning in the third trimester, fetal blood cells are exposed to actively-transported IgG antibody. Thus, we speculated that fetal blood cells would require expression of one or more complement regulators by the early third trimester. Using flow cytometry and Western blots, we have demonstrated the presence of three important complement regulatory proteins in the circulating blood cells of human fetuses. These findings are consistent with the putative biological role of the cell-surface complement regulatory proteins.

Antigens, CD↗
PubMed1997

Different expression and mobilisation of the complement regulatory proteins CD35, CD55 and CD59 in neonatal and adult neutrophils.

We investigated the expression and the N-formyl-methionyl-phenylalanine (fMLP)- and interleukin-8 (IL-8)-induced mobilisation of the complement regulatory proteins CR1 (CD35), decay-accelerating factor (CD55) and CD59 on neutrophils in neonates and adults. The expression of CD35 on resting neonatal neutrophils was significantly higher than in adults. Both fMLP and IL-8 increased CD35 expression more markedly in adults. CD55 on resting neutrophils in neonates was significantly higher than in adults, but did not further increase upon fMLP stimulation as opposed to adults. The increase in CD59 expression was more pronounced in adult neutrophils and was significantly higher than in neonates after fMLP activation. The addition of the protease inhibitor phenylmethanesulphonyl fluoride during fMLP activation improved the upregulation of CD35 significantly more in neonates, but not CD55 or CD59. This effect could be replaced by human normal sera. These data demonstrate that differences exist between neonatal and adult neutrophils with respect to the expression and mobilisation of functional receptors related to protection from autologous complement lysis and may indicate differences in the efficiency to circumvent complement-mediated cell damage at the inflammatory site.

Adult↗
PubMed1989

Characterization of receptors to the anaphylatoxins on isolated cells.

The anaphylatoxins exhibit three primary functions in vivo, i.e. they induce granulocyte sequestration and adherence, promote spasmogenesis or smooth muscle contraction and exert immunoregulatory influences. C5a receptors have been demonstrated on human neutrophils, human monocytes, rodent macrophages from both the lungs and peritoneal cavity, two mouse macrophage cell lines (RAW 264 and J774.A1) and guinea pig platelets. To date, only guinea pig platelet has been shown to possess C3a receptors. In depth studies with the rat mast cell have demonstrated that both direct and indirect activation mechanisms may be operative in the mast cell; however, neither mechanism appears to depend on receptor-mediated stimulation of these cells.

Anaphylatoxins↗