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PubMed1983

Autoradiographical demonstration of C3b receptor activity on resident peritoneal macrophages.

The present study was performed to evaluate the usefulness of 125I-labelled C3b bound to constituents of sheep erythrocyte membranes (125I-C3b-OR) for the demonstration of C3b receptor activity of resident peritoneal macrophages at the electron-microscopical level. The binding of 125I-C3b-OR to the cells was studied in biochemical and autoradiographical experiments. The amount of cell-associated radioactivity was dependent on the presence of unlabelled aggregated C3b (AC3b) in a dose-response manner, and diminished strongly after functional inactivation of the receptor by trypsin treatment. In addition, it was found that at 4 degrees C most of the label was associated with the cell surface. However, when the incubation temperature was raised from 4 degrees C to 37 degrees C, internalization of the label was observed. These results indicate that 125I-C3b-OR is a suitable agent for further characterization of the C3b receptor-function of resident peritoneal macrophages at the electron-microscopical level.

Animals↗
PubMed1988

Immunohistochemical studies of complement receptor (CR1) in cases with normal sinus mucosa and chronic sinusitis.

The complement receptor (CR1) in the maxillary sinus mucosa of normal patients and in cases of chronic sinusitis was studied with the peroxidase-antiperoxidase, avidin-biotin peroxidase and immunofluorescent methods. CR1 was localized on the ciliary surface and in the cytoplasm of the covering epithelium in both normal controls and the cases of chronic sinusitis. CR1 tended to be denser in the mucosa of chronic sinusitis than in normal mucosa. CR1-binding capacity was also studied with the immunofluorescent method, using C3b-conjugated zymosan. Although CR1 did not bind to C3b in vivo, it was found to bind to C3b in the normal maxillary mucosa when it was treated with C3b-conjugated zymosan. CR1-binding capacity could not be detected in the mucosa from cases with chronic sinusitis, indicating that CR1 was already bound to activated C3b in these cases.

Chronic Disease↗
PubMed1986

Immunohistological study of histiocytic necrotizing lymphadenitis.

Immunohistological study of 18 cases of histiocytic necrotizing lymphadenitis (HNL) demonstrated numerous helper/inducer cells (OKT-4) and suppressor/cytotoxic cells (OKT-8) with activation (Tac) and proliferation (OKT-9) markers, and histiocytes (lysozyme, alpha-1 anti-chymotrypsin, OK-M1) in the affected areas. However, B cells (B-1), NK cells (Leu-7 and Leu-11), complement proteins and receptor (C4 and C3d receptor), and neutrophils (chloroacetate esterase) were scanty or absent in these foci. Activity of NK cells was also decreased in the peripheral blood of 2 cases examined. The results suggest that HNL might be induced by the abnormal T cell-histiocyte response against some causative agents which induce a similar reaction of delayed hypersensitivity type.

Adolescent↗
PubMed1990

Nonsteroidal antiinflammatory drugs exert differential effects on neutrophil function and plasma membrane viscosity. Studies in human neutrophils and liposomes.

Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit neutrophil functions via mechanisms separate from their capacity to inhibit prostaglandin synthesis. We have studied discrete events in the process of signal transduction: NSAIDs but not a related analgesic drug (acetaminophen), inhibited aggregation in response to the chemoattractants f-Met-Leu-Phe (FMLP), leukotriene B4, and C5a. NSAIDs, but not acetaminophen, inhibited binding of radiolabeled FMLP to purified neutrophil membranes. Gpp(NH)p, a GTPase insensitive analog of GTP, also inhibited the binding of FMLP but, paradoxically, enhanced superoxide anion generation and lysozyme release. The inhibition of ligand binding by NSAIDs did not correlate with their capacity to inhibit FMLP-induced increments in diacylglycerol (DG): piroxicam, but not salicylate effectively inhibited appearance of label ([3H]arachidonate, [14C]glycerol) in DG. Finally, NSAIDs exerted differential effects on the viscosity of neutrophil plasma membranes and multilamellar vesicles (liposomes): membrane viscosity was increased by piroxicam and indomethacin, decreased by salicylate, and unaffected by acetaminophen. Thus, the different effects of NSAIDs on discrete pathways are not due to their shared capacity to reduce ligand binding but rather to a capacity to uncouple postreceptor signaling events that depend upon the state of membrane fluidity.

Acetaminophen↗
PubMed1990

Bacterial lipopolysaccharide enhances polymorphonuclear leukocyte function independent of changes in intracellular calcium.

Bacterial lipopolysaccharide (LPS) enhanced expression of C3bi receptors (CR3), phagocytosis of opsonized bacteria, and subsequent hydrogen peroxide (H2O2) production by human polymorphonuclear leukocytes (PMNs). The role of changes in intracellular calcium concentration ([Ca2+]i) in LPS-induced priming was examined by determining the effect of modulators of intracellular calcium on enhanced PMN function, determining the ability of calcium ionophores to reproduce the effects of LPS, and measuring PMN [Ca2+]i following addition of LPS. Inhibition of intracellular calcium-dependent processes with TMB-8 or quin-2 blocked all three measures of LPS-induced priming. LPS did not stimulate an increase in [Ca2+]i, and calcium ionophores failed to reproduce the effect of LPS. Maintenance of [Ca2+]i is necessary for LPS priming, but an increase in [Ca2+]i is not a component of the signal transduction pathway leading to PMN priming by LPS.

Aminoquinolines↗
PubMed1989

Role of intracellular calcium in priming of human peripheral blood monocytes by bacterial lipopolysaccharide.

To determine the role of intracellular calcium ([Ca2+]i) in the priming of monocytes (M phi) by bacterial lipopolysaccharide (LPS), the membrane expression of two functional proteins and phagocytosis and respiratory burst were examined by microfluorimetry. LPS induced a significant increase in HLA-DR and C3bi receptor (CR3) expression within 2 h of its addition to whole blood. The enhanced expression of both antigens by LPS was dose-dependent, with concentrations as low as 0.1 ng/ml producing a response. The involvement of [Ca2+]i was demonstrated by loading isolated M phi with the intracellular calcium chelator quin-2 or the inhibitor of intracellular calcium redistribution TMB-8 prior to addition of LPS. Both compounds inhibited the LPS-induced increase in HLA-DR and CR3 expression. No role for extracellular calcium, for calcium slow channel flux, or for the calcium-calmodulin complex in LPS priming was demonstrated when LPS was added in the presence of EGTA, trifluperazine (TFP), or verapamil. The addition of the calcium ionophores A23187 or ionomycin failed to increase expression of either antigen. Prior exposure to LPS primed M phi for enhanced phagocytosis and respiratory burst activity. These functions were inhibited by TMB-8, but not by TFP or verapamil. Addition of LPS to isolated M phi increased [Ca2+]i by 23% at 30 sec and 42% at 5 min, as measured by the calcium-sensitive, intracellular probe indo-1. These results suggest that intracellular Ca2+ mobilization is necessary, but not sufficient, for LPS-induced priming of human peripheral blood monocytes.

Aminoquinolines↗
PubMed1990

Effects of chemotactic peptide f-Met-Leu-Phe (FMLP) on C3b receptor (CR1) expression and phagocytosis of microspheres by human neutrophils.

FMLP caused maximal upregulation of CR1 on neutrophils at a concentration of 10(-8) M but caused maximal enhancement of CR1-dependent phagocytosis of C3b.IgG-coated microspheres only at a concentration of 10(-6) M. There were positive correlations between FMLP-mediated upregulation of CR1 and FMLP-mediated enhancement of phagocytosis (correlation coefficient = 0.73, slope = 2.2) and between FMLP-mediated upregulation of CR1 and FMLP-mediated increase in total cell-associated microspheres (correlation coefficient = 0.88, slope = 1.3). The phagocytic capacity of both untreated and 10(-6) M FMLP-treated neutrophils was completely inhibited by fluid phase C3b and partially inhibited by aggregated IgG. The data suggest that CR1 upregulation is required but is not sufficient for maximal phagocytosis by the leukocytes. The data also suggest that FMLP at the higher concentrations may impart a phagocytic function to CR1, activate other phagocytic receptors, elicit phagocytosis-inducing mediators or may elicit a separate mechanism of phagocytosis. During the study, it was observed that there was considerable individual variation among different neutrophil preparations with respect to CR1 expression and binding and phagocytic capacity.

Humans↗
PubMed1993

Terpenes enhance metabolic activity and alter expression of adhesion molecules (Mac-1 and L-selectin) on human granulocytes.

Granulocytes from healthy blood donors were exposed to terpenes dissolved in ethanol. Flow cytometry was used to measure the expression of the cell surface receptors Mac-1 L-selectin, and CR1, which were detected by monoclonal antibodies. The phagocytic activity was determined by using C3b-coated yeast particles as prey. The metabolic activity was measured by determining the intracellular hydrogen peroxide production using dichlorofluorescein diacetate. After terpene exposure the expression of Mac-1 and CR1 increased (P < 0.001 and P < 0.01, respectively) and the expression of L-selectin decreased (P < 0.001). There was also an increased metabolic activity (P < 0.001). The cell viability, the cell count, and the phagocytic activity remained unchanged. These findings suggest that terpene exposure triggers the granulocytes to a higher degree of activation in terms of an altered expression of the adhesion molecules and an increased metabolic activity.

Cell Adhesion↗
PubMed1993

Presence of serum modulates expression of complement receptor type 1 (CR1) on human granulocytes after quartz exposure.

We have investigated the interaction between granulocytes and quartz with respect to the expression of complement receptor type 1 (CR1) and the presence of normal human serum (NHS). Quartz down-regulates selectively CR1 on activated granulocytes. This down-regulation is abolished in the presence of both NHS and heat-inactivated NHS (NHS56) but not human albumin. When quartz was preincubated with NHS (quartz-NHS) before exposure to activated granulocytes, a down-regulating effect was observed in contrast to preincubation with NHS56, which did not induce a down-regulation. Preincubation with cytochalasin B reduced the down-regulation of quartz-NHS, indicating a cytoskeleton-dependent internalization of the receptor. The serine protease inhibitor PMSF partly reduced this down-regulation. Our results indicate that the presence of NHS in the alveolar space influences the interaction between quartz and recruited granulocytes with respect to CR1 expression. Since CR1 is an important opsonin receptor and soluble CR1 can modulate the inflammatory response, this may be of importance in the inflammation and fibrosing process induced by quartz in the alveolar space and lung interstitium.

Blood Physiological Phenomena↗
PubMed1990

Comparison of abilities of recombinant interleukin-1 alpha and -beta and noninflammatory IL-1 beta fragment 163-171 to upregulate C3b receptors (CR1) on human neutrophils and to enhance their phagocytic capacity.

Both recombinant IL-1 alpha and -beta caused an upregulation of C3b receptors (CR1) on human neutrophils and caused a receptor-mediated enhancement of phagocytosis of C3b.IgG-coated microspheres by these leukocytes. The alpha and beta forms of the recombinant cytokine were of comparable potency regarding CR1 upregulation, although both generally had less than 25% of the potency of FMLP in this respect. Recombinant IL-1 beta was slightly more potent than the alpha form of the cytokine regarding phagocytosis of opsonized microspheres and, again, both forms were less potent than FMLP in causing an enhancement of phagocytosis by neutrophils. The synthetic noninflammatory immunostimulatory nonapeptide corresponding to residues 163-171 of IL-1 beta was completely inert with respect to upregulation of CR1 on neutrophils and the enhancement of phagocytosis by these cells. Thus this domain in the intact IL-1 beta molecule apparently is not involved in CR1 upregulation and the ensuing enhancement in phagocytosis by neutrophils, although it is apparently important in the immunostimulatory activity regarding the proliferation of lymphocytes.

Antigens, CD↗
PubMed1984

Deficiency in C3b receptors on neutrophils of patients with chronic granulomatous disease and hyperimmunoglobulin-E recurrent infection (Job's) syndrome.

C3b receptor (CR1) expression by neutrophils (PMNs) and erythrocytes (Es) from patients with chronic granulomatous disease (CGD) or with hyper-IgE, frequent infection (Job's) syndrome was compared with that of control subjects. The control subjects consisted of one group of patients with infections and a second group of normal, healthy individuals. Three quantitative assays were used: rosette formation with C3b-coated cellular intermediates (EAC43b), binding of radiolabeled monoclonal anti-CR1 ([125I]anti-CR1) to PMN surfaces, and binding of the antibody to nonidet P-40 (NP-40) extracts of PMNs and Es in an immunoradiometric assay. Rosette formation by the PMNs of five male CGD patients was about 50% of that of paired normal control subjects, whereas the rosette formation of three female CGD patients was similar to that of the control subjects. Surface binding of [125I]anti-CR1 to PMNs of 10 CGD patients was about half that of the normal subjects (mean percent binding was 2.33% for the CGD patients vs. 3.86% for the normal subjects, giving a difference of -1.53 +/- 0.22%, P less than 0.001 by the paired-sample t test). The degree of PMN binding was similarly low for both the male and the female CGD patients. Conversely, the binding of anti-CR1 to the PMNs of 11 infected control patients appeared to be similar to that of the normal subjects (4.51% for the patient vs. 4.21% for the paired normal subjects). The infected control group originally included four Job's syndrome patients, and when this subgroup was analyzed separately, their PMNs were shown to bind significantly less anti-CR1 than did the PMNs of the normal subjects (P less than 0.01 by the paired-sample t test). In contrast, the other infected control patients showed higher-than-normal levels of anti-CR1 binding (P less than 0.05). When compared to that of the normal subjects, the total CR1 quantitated in PMN extracts was also lower than normal in CGD patients (P less than 0.01 and in the PMN extracts of eight Job's syndrome patients tested (P less than 0.01). The PMNs of the other infected control subjects were not significantly different from those of the normal subjects in total CR1 expression. Extracts of Es from Job's syndrome patients also had fewer than normal CR1 (P less than 0.02). On the other hand, CR1 levels in E extracts from the CGD patients and the other control patients were similar to those in the normal control subjects. Quantitations of C3, C4, and factor B were normal in CGD.(ABSTRACT TRUNCATED AT 400 WORDS)

Antigen-Antibody Complex↗
PubMed1986

Effects of systemic in vivo interleukin-2 (IL-2) reconstitution in patients with acquired immune deficiency syndrome (AIDS) and AIDS-related complex (ARC) on phenotypes and functions of peripheral blood mononuclear cells (PBMC).

In the context of a clinical phase I/II therapy study with recombinant interleukin-2 (rIL-2), we monitored immunological alterations in four patients with acquired immune deficiency syndrome (AIDS) and three patients with AIDS-related complex (ARC). By determining the surface phenotypes and in vitro functions of peripheral blood mononuclear cells (PBMC) before, during, and after treatment with rIL-2, we observed transient changes in all important leukocyte subpopulations, a minor restoration of immune reactivity in vitro, and an improvement in skin reactivity in vivo. In particular, we found a transient increase in C3b receptor-mediated monocyte activation in ARC patients; no influence of therapy on the otherwise intact LPS-induced interleukin-1 production in vitro; in some patients a transient corrective influence on the high pretherapeutic immunoglobulin secretion of B cells and their nonresponsiveness to pokeweed mitogen; low T-cell responses to soluble antigens and alloantigens, which were partially restored during rIL-2 treatment in ARC patients and in one AIDS patient; defective NK activity in PBMC of two AIDS patients, which was found to be restored when measured at the end of rIL-2 therapy; and a rather constant phenotypic pattern of PBMC in each patient during therapy except for the decreasing proportion of OKT9-positive lymphocytes in AIDS patients, the increasing proportion of Leu8-Leu3a+ lymphocytes in all patients, and in particular, the transient significant decrease in the Leu7+/OKT3+ ratio, which pretherapeutically was very high in AIDS patients (0.78 +/- 0.21) and high in ARC patients (0.48 +/- 0.06) as compared to healthy controls (0.18 +/- 0.08).

Acquired Immunodeficiency Syndrome↗
PubMed1982

Complement does not play a role in promoting Babesia rodhaini infections in Balb/C mice.

A critical role of C3 and the C3b receptor for the erythrocyte invasion and the development of the parasitemia of B. rodhaini in rats has been described recently (Jack and Ward 1980a). In the present study the influence of the C system on B. rodhaini infection in Balb/C mice is documented. Depletion of serum C3 to less than 5% of the normal level by treatment of mice with CoF, the C3 inactivator isolated from cobra venom, did not affect the course of B. rodhaini parasitaemia. Treatment of mice with trypan blue, a reagent that inactivates the C3b receptor on human polymorphonuclear leukocytes, inhibited the development of parasitemia. However, when B. rodhaini parasitized erythrocytes were incubated in vitro with trypan blue and subsequently tested for the in vivo and in vitro replication of the parasites, this old-fashioned therapy for babesiosis in cattle showed its babesiacidal activity. This indicates that the inhibition of parasite development by trypan blue is caused by its parasitotoxicity. These data suggest that the C system does not play an essential role in the development of B. rodhaini infection of the Balb/C mouse.

Animals↗
PubMed1981

C3 modified at the thiolester site: acquisition of reactivity with cellular C3b receptors.

Isolated human C3 protein has been reported to have variable affinity for cellular C3b receptors. The question was investigated therefore as to whether native C3 or a derivative form of the protein exhibits receptor affinity. It was found that native C3 lacks the ability to react with C3b receptors. However, C3 modified at the thiolester site, either by treatment with chaotropic agents or methylamine or by freezing and thawing, expressed inhibitory activity in the C3b-mediated rosetting assay or immune adherence. The extent of inhibition was comparable to that caused by C3b. The ability of modified C3 to react with cellular C3b receptors constitutes an additional functional property of C3b-like C3.

Animals↗
PubMed1986

Deficiency of erythrocyte C3b receptor (CR1) in AIDS and AIDS-related syndromes.

The expression of C3b receptors (CR1) on erythrocytes of gay men at various levels of risk for AIDS was studied. Fourty-nine heterosexual male controls had a mean (X) +/- standard deviation of 516 +/- 136 CR1 per erythrocyte (CR1-3); 17 asymptomatic gay men had X = 423 +/- 156, 16 gay men with one AIDS-related complex (ARC) symptom or sign had X = 342 +/- 154, 9 patients with ARC had X = 252 +/- 76, and 14 gay men with AIDS had X = 173 +/- 76 CR1-E. The patients with ARC and AIDS had a highly significant decrease in CR1-E when compared with normal individuals (p = less than 0.001) and studies of families of 4 AIDS patients suggest that this defect is acquired.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Urocanic acid suppresses the activation of human neutrophils in vitro.

Exposure to ultraviolet (UV) light impairs the function of inflammatory cells. Urocanic acid (UCA) in an stratum corneum has been suggested as a mediator in the immunosuppression of lymphoid cells detected after irradiation with UVB (UV wavelengths 280-320 nm). In this study, we examined the effects of the two UCA isomers, trans and cis UCA on human polymorphonuclear leukocytes, neutrophils. It was found that treatment of cells with either trans of cis UCA isomers inhibited the opsonized zymosan-induced respiratory burst activity, measured with luminol-enhanced chemiluminescence assay. Both isomers were also able to partially block the up-regulation of complement receptors 1 (CR1; CD35) and 3 (CR3; CD11b/ CD18) in N-formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated neutrophils. These results indicate that the isomerization of trans UCA to cis UCA is not essential for the action of UCA on neutrophils. Neither of the UCA isomers were found to induce cyclic AMP (cAMP) formation in 3-isobutyl-1-methylxanthine treated cells, suggesting that the activation of adenylate cyclase cAMP system is not involved in UCA provoked suppression of neutrophils. It is concluded that the function of UCA may be protective, to suppress the activation of human neutrophils in inflamed, sunburned epidermis.

Cyclic AMP↗
PubMed1984

Characterization of the third component of pig complement and its utilization in a C3b receptor study.

The third component of the pig complement system (C3) was isolated in hemolytically active form and characterized. The C3 component is a beta-globulin with the molecular weight of 191,000 and is composed of 2 non-identical polypeptide chains of Mr 112,000 and 74,000. The isolated C3 can be used for the detection of the C3b receptor on the membranes of heterologous peritoneal macrophages.

Animals↗
PubMed1988

Clearance of cryoglobulins in man.

From the foregoing it is evident that the defective clearance of immune complexes may contribute to tissue damage seen in patients with cryoglobulins. Hypocomplementaemia, decreased erythrocyte CR1, and the nature of the immune complexes may all contribute to decreased binding of immune complexes to erythrocytes with the potential consequence of increased availability for deposition and decreased processing of immune complexes. In addition, in type II cryoglobulinaemia the nature of the immune complex namely IgM RF/IgG complexes, has been shown in some circumstances to fix C3 and C4 inefficiently in spite of detectable fluid phase complement activation. The poor C3 fixation results not only in decreased transport by erythrocytes to the RES but also in inefficient removal of immune complexes by phagocytic cells, since the Fc receptor on these cells would be acting alone without the synergy of occupied complement receptors. Persistence of immune complexes in tissues in these circumstances has two potential consequences. First, the multivalency of IgM may contribute to enlargement of these immune complexes in situ by successive trapping of antigen and antibody complexes; this process may be aided by local factors such as low temperature at the peripheries and increased protein concentration in glomerular capillary loops, which favour "cryo" precipitation. The higher avidity of RF for IgG that is surface bound rather than monomeric would also favor immune complex formation in these circumstances. Second, although there is no opsonization of the immune complex complement activation results in bystander fixation of C4 and C3 to the surrounding tissues resulting in tissue injury.

Antigen-Antibody Complex↗