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PubMed1991

IgA-mediated inhibition of human leucocyte function by interference with Fc gamma and C3b receptors.

The inhibitory effects of IgA from human colostrum, and IgA1 and IgA2 from human serum on the chemiluminescence (CL) response and phagocytosis of polymorphonuclear leucocytes (PML) to Staphylococcus epidermidis and the CL response to formylmethionyl-leucyl-phenylalanine (FMLP) were studied. The dose-dependent inhibition of the luminol-mediated CL response of human PML to the bacteria was observed in the presence of more than 0.1 mg/ml IgA from both colostrum and serum. The preincubation of PML with a solution of IgA enhanced the suppressive effect of IgA on the cells. Removal of IgA from the reaction mixture after preincubation resulted in recovery, with time, of the response of PML to the bacteria. The bacteria treated with IgA did not give rise to any inhibition of the response. The CL response of PML to FMLP was not affected by the presence of IgA in the reaction mixture. The decrease of phagocytic activity of PML in the presence of IgA resulted in a decrease of NADPH oxidase activity of PML after stimulation with the bacteria as compared with the absence of IgA. The effect of IgA on the receptors of Fc and C3b (CR1) on the surface of PML was measured by monitoring erythrocyte-antibody (EA) or erythrocyte-antibody-complement (EAC) rosette formation and by direct and indirect immunofluorescence techniques using anti-CR1 antibody and Fc-specific antibodies. The presence of IgA in the reaction mixture led to a quantitative decrease in CR1 and the ability to bind IgG to the surface of PML.

Antigens, Differentiation↗
PubMed1990

Granulocyte-macrophage colony-stimulating factor increases synthesis and expression of CR1 and CR3 by human peripheral blood neutrophils.

Polymorphonuclear leukocytes (PMN) constitutively synthesize various plasma membrane proteins including CR1(3) (CD35), CR3 (or Mac-1) alpha-chain (CD11b) and MHC class I. PMN are also able to up-regulate rapidly the expression of CR1 and CR3 to the plasma membrane in response to agonists such as FMLP. To determine whether constitutive PMN translation was static or up-regulatable, PMN were cultured in the presence or absence of the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) for 8 h. CR1, CR3 and class I proteins immunoprecipitated from lysates of 35S-methionine pulse-labeled PMN were resolved by SDS-PAGE, fluorographed and quantified by densitometry. GM-CSF-treated PMN synthesized 4.5-fold more class I protein, 3.7-fold more CR1, 2.4-fold more CD11b and 3.4-fold more CR3 beta-chain (CD18), compared with untreated control cells. Actinomycin D treatment of replicate samples of PMN decreased the amount of these proteins synthesized by each group of PMN from 30 to 90%, implying that continued translation was required for the increases in protein synthesis. Nascent CR and class I proteins were inserted into the plasma membrane of PMN, thereby supplementing the molecules already expressed on the cell surface. In addition to these longer term effects of GM-CSF, we observed its acute up-regulatory effects on PMN. GM-CSF induced a five- to 12-fold increase in the expression of CR1 and CR3 on the PMN cell surface within 30 min. These increases were both dose- and time-dependent with maximum up-regulation occurring at 25 pM and at 30 min. In contrast to the long term biosynthetic events, this rapid up-regulation was not dependent on protein synthesis but was due instead to mobilization of CR from intracellular compartments similar to those up-regulated by FMLP. These results demonstrate that PMN can respond to microenvironmental stimuli such as GM-CSF both by rapidly up-regulating and increasing translation and expression of functionally important plasma membrane proteins.

CD18 Antigens↗
PubMed1990

Phenotypic markers of lymphocyte and mononuclear phagocyte activation within rheumatoid nodules.

We investigated rheumatoid subcutaneous nodules using monoclonal antibodies recognizing functional determinants on mononuclear phagocytes (Mph) and lymphocytes. Mph at the center of rheumatoid nodules showed strong expression of the leukocyte intergrins CR3 and p150,95 which would be consistent with the presence of a central chemotactic stimulus. Mph expression of FcR1, a gamma interferon regulated molecule, was decreased in 5/13 cases despite strong expression of MHC class II. There was a variable unstructured infiltrate of T lymphocytes, a majority of which were CD8 positive. Lymphocytes showed increased MHC class II expression but interleukin 2 receptor expression was low. We discerned no relationship between the number, distribution or phenotype of the T cell infiltrate and the phenotype of the predominant Mph population.

Adult↗
PubMed1988

Vitronectin (S protein) augments the functional activity of monocyte receptors for IgG and complement C3b.

An arginine-glycine-aspartic acid sequence (RGD in the single letter code for amino acids) is present in the cell attachment site of both vitronectin and fibronectin. Inasmuch as fibronectin and synthetic peptides containing RGD enhance ingestion of opsonized particles by monocytes, we investigated the effects of vitronectin on phagocytosis by monocytes of sheep erythrocytes bearing IgG (EA) or complement C3b (EC3b). Peripheral blood monocytes were isolated by countercurrent elutriation and allowed to adhere to slides that had been coated with either vitronectin or fibronectin. Next, EA or EC3b were incubated with the adherent monocytes, and phagocytosis was subsequently quantified. Vitronectin caused the same dose dependent increase in phagocytosis as fibronectin. The augmentation of phagocytosis of EA induced by vitronectin could be inhibited by the F(ab')2 fragments of anti-vitronectin IgG but not by preimmune F(ab')2. The maximum phagocytosis of EA induced by vitronectin could not be enhanced by the addition of fibronectin, suggesting that vitronectin and fibronectin act on the same population of monocytes and that the two proteins stimulate the same mechanism through which the enhanced phagocytosis is mediated. Fibronectin and vitronectin caused a tenfold increase in the attachment of EC3b to monocytes, but phagocytosis was augmented minimally. These studies demonstrate that vitronectin modulates interactions between monocytes and opsonized particles.

Complement C3b↗
PubMed1988

The human leukocyte adhesion glycoprotein Mac-1 (complement receptor type 3, CD11b) alpha subunit. Cloning, primary structure, and relation to the integrins, von Willebrand factor and factor B.

Mac-1 (CD 11b/CD18) is a leukocyte adhesion heterodimeric glycoprotein which functions both as a receptor for iC3b (CR3) and in several cell-cell and cell-substrate adhesive interactions. We describe full-length cDNA clones for the alpha subunit of Mac-1. Mac-1 alpha subunit message was detected in blood monocytes and phorbol-12-myristate acetate-induced myeloid cell lines, but not in cells of the T or B lineages, correlating with Mac-1 protein surface expression. The alpha subunit of Mac-1 is a transmembrane protein of 1137 residues with a long extracellular domain (1092 residues) and a 19-amino acid cytoplasmic tail. The extracellular domain contains three putative divalent cation-binding sequences and 19 potential N-glycosylation sites. The amino acid sequence of Mac-1 alpha shows that it is a member of the integrin superfamily; Mac-1 alpha shows 63% identity to the alpha subunit of the leukocyte adhesion glycoprotein p150.95 and 25% to the alpha subunits of the extracellular matrix receptors platelet glycoprotein IIb/IIIa, the fibronectin receptor, and the vitronectin receptor. The Mac-1 alpha subunit putative divalent cation-binding sites and the flanking regions exhibit a high degree of identity both to the p150.95 alpha subunit (87% identity at the amino acid level) and to the rest of the integrin alpha subunits (38%). The alpha subunit of Mac-1, like the p150.95 alpha subunit, contains a domain of 187 amino acids in the extracellular region which is absent in other integrins. This leukocyte or "L" domain is homologous to the A domains of von Willebrand factor, which in turn are homologous to regions of the C3-binding proteins factor B and C2. These findings draw attention to this region of Mac-1 as a potential binding site for iC3b.

Amino Acid Sequence↗
PubMed1989

Human liver Kupffer cells express CR1, CR3, and CR4 complement receptor antigens. An immunohistochemical study.

The expression of complement receptor antigens by human Kupffer cells (KC) was investigated by immunohistochemical techniques in seven normal human liver biopsies. Polyclonal and monoclonal antibodies were revealed by double labeling of cells using indirect immunofluorescence and immunoenzymatic techniques or by using double immunoenzymatic techniques. In most experiments, one antigen was revealed by streptavidin-biotin-peroxidase complexes whose reaction product was examined by light microscopy and the second antigen stained using the alkaline phosphatase antialkaline phosphatase method visualized by fluorescence microscopy using fluorescein isothiocyanate or tetramethylrhodamine isothiocyanate filters. KC were identified using monoclonal antibody EBM11 that recognizes 100% of KC in hepatic lobules and was paired with each antibody directed against complement receptors. CR1 and CR3 (alpha- and beta-chains) were found to be the predominant receptor antigens expressed by human KC. CR4 (p150,95) was expressed on all KC, but staining with anti-CR4 monoclonal antibodies was consistently weaker than that observed with anti-CR3 antibodies. No staining of KC was observed with anti-CR2 (CD 21) antibodies. Expression of CR1, CR3, and CR4 complement receptors on KC provides the cells with an optimal capacity to bind and phagocytize particles or immune complexes coated with any type of ligands for C3 receptors.

Antibodies, Monoclonal↗
PubMed1989

[Effect of prodigiozan on the antibody-dependent cytotoxicity of neutrophils in chronic myeloid leukemia].

Decreased levels of neutrophils, Fc- and C3-expressing receptors, oxygen-dependent metabolism as well as antibody-dependent cytotoxicity of these cells to target cells were identified in advanced chronic myeloid leukemia, particularly, in blast crisis. Treatment with cytostatic agents resulted in further decrease in said parameters. However, treatment with prodigiozan was followed by improvement in cell functioning.

Adjuvants, Immunologic↗
PubMed1989

Effect of fibronectin on C3b and Fc receptor-mediated phagocytosis by peripheral blood monocytes in uraemic patients.

The influence of human fibronectin was evaluated on the phagocytosis in vitro of C. albicans (C3b receptor-mediated) and IgG antibody-coated sheep erythrocytes (Fc receptor-mediated) by the peripheral blood monocytes of 40 uraemic patients undergoing periodic haemodialysis. Some nutritional parameters (albumin, transferrin, C4, C3, haematocrit, lymphocyte count, height and bodyweight) were also evaluated. Results showed significantly decreased plasma fibronectin (P less than 0.001) and reduced C3b receptor (R)- and FcR-mediated phagocytosis in uraemic patients (P less than 0.001). A strict correlation was found between fibronectin and C3bR-mediated phagocytosis (P less than 0.001) and between fibronectin and FcR-mediated phagocytosis (P less than 0.05). In 20 patients with decreased fibronectin concentrations and reduced phagocytic function, the in vitro incubation of peripheral blood monocytes with 50 micrograms/ml of purified fibronectin significantly enhanced C3bR-(P less than 0.001) but not FcR-mediated phagocytosis. Study of nutritional parameters in the uraemic patients revealed that values of fibronectin, C3, IgG and albumin were significantly reduced. Fibronectin correlated significantly (P less than 0.001) with C3. A good relationship (P less than 0.05) was also found between the plasma fibronectin and bodyweight loss. A greater incidence of infectious disease was observed in patients with decreased plasma fibronectin than in uraemic patients with normal values (P less than 0.05). The results suggest that a decrease in plasma fibronectin in uraemic patients could impair the peripheral blood monocyte phagocytic capacity and be potentially dangerous, predisposing the patient to infections. The determination of fibronectin concentration in these patients may, therefore, have a potential value as an indicator of peripheral blood monocyte phagocytic function.

Adult↗
PubMed1989

Quantification of macrophage cell surface molecules in rheumatoid arthritis.

The response of macrophages to stimulation by interferon-gamma (IFN-gamma) in vitro is characterized by an increase in the cell surface expression of MHC class II HLA-DR antigen (HLA-DR) and the high-affinity Fc-receptor for immunoglobulin G (FcRI) while the expression of the C3b-receptor (CR1) is reduced. Based on these observations, we have examined further the possibility that IFN-gamma may modulate the activation of mononuclear phagocytes (Mph) in patients with rheumatoid arthritis (RA). As reported by others, we found low levels of IFN-gamma in the synovial fluid of these patients (less than 0.3 IU/ml using radioimmunoassay). As an alternative means of establishing whether Mph are influenced by levels of IFN-gamma too low to measure directly, we have quantified the expression of membrane associated HLA-DR, FcRI and CR1 on cell populations isolated from synovial fluid and peripheral blood. The expression of these molecules by Mph is known to be influenced by IFN-gamma. We found that Mph isolated from the synovial fluid of patients with RA showed a significantly increased HLA-DR expression. Significantly less CR1 was associated with the synovial fluid Mph than with peripheral blood monocytes. However the expression of the FcRI by the synovial fluid Mph and peripheral blood monocyte populations was similar. The quantitative changes in HLA-DR and CR1 expression by synovial fluid Mph (but not those of FcRI) were consistent with those seen following IFN-gamma activation of monocytes in vitro. While these results indicate that IFN-gamma may have a role in activating the Mph present in synovial fluid, the apparent independent regulation of FcRI observed suggests other mediators may also be involved.

Antigens, Differentiation↗
PubMedDate not supplied

Polymorphonuclear functions in patients with mixed connective tissue disease.

Polymorphonuclear leukocytes (PMNs) from 29 patients with mixed connective tissue disease (MCTD) were studied "in vitro" for their phagocytic and chemotactic function as well as for granulocyte alkaline phosphatase (GAP) activity. Fc-receptor expression detected by EA-rosette formation was comparable to the control. Yeast-phagocytosis, C3b-receptor mediated phagocytosis and chemotaxis of PMNs, however, significantly decreased in MCTD. At the same time, photometric measure of alkaline phosphatase activity indicated a nearly two fold increase in PMNs from patients with MCTD. Although no correlation was found between PMN functions and the activity of the disease, PMN disorders may play a role in pathogenesis of these connective tissue disorders.

Adult↗
PubMed1989

An immobile subset of plasma membrane CD11b/CD18 (Mac-1) is involved in phagocytosis of targets recognized by multiple receptors.

CD11b/CD18 is a heterodimeric leukocyte surface receptor which functions in both C3bi-ligand binding and homotypic and heterotypic cell adherence. We have examined the effect of several anti-CD11b/18 mAb on phagocytosis of IgG (EIgG) or complement (EC4b) opsonized erythrocytes by polymorphonuclear leukocytes (PMN) and monocytes. F(ab')2 of two mAb (IB4, an anti-beta-chain mAb and Mo-1 an anti-alpha-chain mAb), inhibited both phagocytosis of EIgG and phorbol ester-stimulated phagocytosis of EC4b by PMN and monocytes. These F(ab')2 inhibited the binding of EIgG to monocytes, but they had no effect on binding of EIgG to PMN, or EC4b to either phagocyte. In addition, IB4 inhibited phorbol-ester stimulated phagocytosis of sheep E opsonized with C component 3bi (EC3bi) without inhibiting rosetting of these same targets. These data separate the anti-phagocytic effect of these mAb from effects on phagocyte-target adherence. When PMN were adherent to an anti-CD11b/CD18 F(ab')2-coated surface, EC3bi binding was abolished, but phagocytosis of EIgG or EC4b was unaffected. Subsequent addition of fluid- phase IB4 or Mo-1 F(ab')2 inhibited phagocytosis of EIgG or EC4b by the adherent cells. This suggested that the CD11b/CD18 involved in C3bi rosetting were mobile in the membrane, whereas those involved in phagocytosis of EIgG or EC4b were not. Cytochalasin treatment of PMN during adherence to F(ab')2-coated plates decreased both apical expression of CD11b/18 and subsequent ingestion of EIgG by 70%, suggesting that microfilaments are important in maintaining immobile CD11b/18 on the apical PMN surface. We conclude that there are functionally distinct populations of CD11b/CD18 on monocytes and PMN: one involved in C3bi rosetting and another involved in the process of phagocytosis mediated via several different receptors. CD11b/18 is not required for optimal target binding in all cases, but is always required for ingestion. As with several other integrins, the CD11b/18 molecules involved in phagocytosis have a functional association with the cell cytoskeleton.

Antibodies, Monoclonal↗
PubMed1989

Recombinant human granulocyte colony-stimulating factor as an activator of human granulocytes: potentiation of responses triggered by receptor-mediated agonists and stimulation of C3bi receptor expression and adherence.

Recombinant human granulocyte colony-stimulating factor (rhG-CSF) enhanced superoxide release and membrane depolarization in parallel in human granulocytes stimulated by the receptor-mediated agonists, N-formyl-methionyl-leucyl-phenylalanine and wheat germ agglutinin, but not by the Ca2+ ionophore ionomycin and phorbol myristate acetate, which bypass the receptors to stimulate the cells. The optimal effect was obtained by pretreatment of cells with 25 to 50 ng/mL (1.3 to 2.6 nmol/L) rhG-CSF for 10 minutes at 37 degrees C. rhG-CSF produced by bacteria and mammalian cells had identical biological effects on a molar basis. rhG-CSF neither affected stimulus-induced increase in cytoplasmic free Ca2+ nor changed the number and affinity of N-formyl-methionyl-leucyl-phenylalanine receptors. The priming effect of rhG-CSF was temperature dependent and did not require new protein synthesis. rhG-CSF increased the expression of C3bi receptors on human granulocytes and enhanced granulocyte adherence to nylon fiber. The optimal effect was obtained by pretreatment of cells with 25 to 50 ng/mL rhG-CSF for 30 minutes at 37 degrees C. rhG-CSF had no effect on human monocytes. These findings demonstrate that rhG-CSF can selectively stimulate mature granulocyte functions.

Calcium↗
PubMed1988

Effect of respiratory infections caused by bovine herpesvirus-1 or parainfluenza-3 virus on bovine alveolar macrophage functions.

Calves, 90 to 130 days old, were inoculated with bovine herpesvirus-1 (BHV-1) or parainfluenza-3 (PI-3) virus. Pulmonary lavage specimens obtained from calves before virus inoculation contained 98% alveolar macrophages (AM) and 1% neutrophils. Six days after inoculation, the mean percentage of neutrophils in lavage specimens had significantly increased to 7.9 +/- 6.0% in BHV-1-inoculated calves and to 18.3 +/- 9.9% in PI-3 virus-inoculated calves, reflecting viral-induced pulmonary inflammation that was confirmed histologically. Approximately 75% of AM obtained before virus inoculation had Fc surface receptors, and 60% had C3b receptors. Six days after inoculation, the percentage of AM with Fc and C3b receptors was significantly reduced to 69.7 +/- 8.6% and 27.1 +/- 19.8%, respectively, in BHV-1-inoculated calves and to 67.8 +/- 15.4% and 38.8 +/- 23.2%, respectively, in PI-3 virus-inoculated calves. Alveolar macrophages obtained after virus inoculation were significantly impaired in their ability to phagocytize opsonized Staphylococcus epidermidis, but were able to kill ingested bacteria. Alveolar macrophage dysfunctions caused by BHV-1 or PI-3 respiratory infection did not differ appreciably.

Animals↗
PubMed1985

The expression of Fc and complement receptors in young, adult and aged mice.

Age-dependent changes in the expression of Fc receptors (FcR) for different isotypes of immunoglobulins and receptors for C3b, C5b and C3bi fragments of complement on the membranes of peritoneal macrophages were studied with mice of different ages. An age-related increase in expression of Fc receptors for IgM, IgE, IgA, IgG2b and IgG3, and a decrease in the expression of Fc receptors for IgG1 was observed. The expression of FcR on macrophages of donors of different ages corresponded with Fc-receptor mediated phagocytosis. The highest number of C3b-binding macrophages was found in aged mice, in contrast to low numbers of C3bi-binding macrophages at this age. The percentage of C5b-binding macrophages was lowest in adult animals. We also observed effective inhibition of binding of the C3b component of complement by preincubation of macrophages with aggregated IgG and vice versa. These observations suggest that fluctuation in expression of Fc but not C receptors may be important to the generalized changes that occur in macrophage function during development and ageing.

Aging↗
PubMed1985

The induction of functional mononuclear and multinuclear macrophages in murine brugian filariasis: morphological and immunological properties.

This present study describes the ontogeny and morphology of mononuclear and multinuclear macrophages in murine Brugia pahangi infections. Intraperitoneal infection with L 3 resulted in the development of adult worms and the production of microfilariae in many mice; however, all worms were usually removed by 100 days post infection (p.i.). The infection induced predominantly mononuclear and multinuclear macrophage responses in the peritoneal cavity, with maximum numbers of peritoneal cells being achieved by 8-12 weeks p.i. and at this time some 20% of the macrophages were multinucleated. Lymphocyte numbers were also increased during infection. The reactions around the filariae involved macrophages (both single and multinucleated), eosinophils, fibroblasts and the laying down of collagen. Most worms were involved in these cellular reactions by 5-6 weeks p.i., with the multinuclear macrophages generally seen lying close to the parasites. All stages of parasites developed vacuolar internal changes early in their degeneration with calcification being a later change. The destruction and removal of the sheath was not apparently a prerequisite for degeneration of the body of microfilariae. Rosetting techniques showed that 75% of peritoneal cells (macrophages) in infected animals possessed Fc receptors compared with 32% of those in uninfected mice, and for C3 receptors the respective results were 35% and 5%. The multinuclear cells possessed both types of receptors at levels similar to those of mononuclear macrophages. Likewise both cell types were found to readily phagocytose yeast and latex particles, as well as staining positively for non-specific esterases.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

In vivo and in vitro effects of doxycycline on leucocyte membrane receptors.

Tetracyclines, particularly doxycycline, have adverse effects on granulocyte function in vitro. We have examined the effects of doxycycline on membrane receptors for IgG (Fc gamma-R) and C3b (C3b-R) on granulocytes and lymphocytes, as well as on the sheep erythrocyte receptor (E-R) on T lymphocytes. Acne patients given doxycycline orally had a lower percentage of Fc gamma-R positive granulocytes (57%) than before treatment (80%) or compared to healthy controls (81%). Following in vitro doxycycline incubation, normal granulocytes showed decreased levels of Fc gamma-R positive cells. This effect was counteracted by the addition of magnesium during incubation. The deleterious effect of doxycycline on granulocyte functions may be due to decreased levels of Fc gamma-R bearing granulocytes. Doxycycline in vivo or in vitro had no significant effect on the proportion of C3b-R bearing granulocytes or lymphocytes or the T lymphocyte percentage. After in vitro irradiation with light at 340-380 nm, however, both granulocytes and lymphocytes preincubated with doxycycline showed up to 50% decrease in Fc gamma-R bearing cells, while control cells without doxycycline were unaffected.

Acne Vulgaris↗
PubMed1986

The endothelial surface and responses to injury.

Pulmonary microvascular endothelial cells are known to play an active role in the events that lead to vascular damage in the inflammatory response. The endothelial surface, normally immunologically privileged and very actively antithrombogenic, can respond to certain stimuli, generally injurious, by becoming strongly procoagulant and by expressing Fc and C3b receptors. Like macrophages, activated endothelial cells can provide a common source and substratum for combined hemostatic and complement-linked reactions. Such transformations of endothelial functions may involve alterations in the endothelial glycocalyx and, in addition, may be important for the entrapment and disposal of phagocytosed particulates. What is clear is that it is not simply absence of endothelium that has a bearing on the outcome of inflammatory stimuli but that structural and functional responses of the endothelial surface to injury, resulting in altered expression of hemostatic and immunologic potential, may have an important bearing on the role of the endothelium in the regulation of microvascular permeability.

Animals↗