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PubMed1995

Priming of human polymorphonuclear neutrophilic leukocytes by insulin-like growth factor I: increased phagocytic capacity, complement receptor expression, degranulation, and oxidative burst.

Insulin-like growth factor I (IGF-I) is a GH-dependent peptide regulating mammalian growth that seems to be of importance for the normal development and function of the immune system. Polymorphonuclear neutrophilic leukocytes (PMNLs) are terminally differentiated phagocytes essential for host defense, and in the present study, recombinant human IGF-I was shown to be a powerful primer of mature human PMNLs. IGF-I augmented the PMNL phagocytosis of both immunoglobulin G-opsonized Staphylococcus aureus and complement-opsonized Candida albicans. In addition, the growth factor increased PMNL complement receptor expression [complement receptors 1 (CD35) and 3 (CD11b)] and primed the cells to stronger f-met-leu-phe-induced degranulation of both specific and azurophilic granules [markers: CD11b, CD35 and CD67 (specific granules); CD63 (azurophilic granules)]. In contrast, IGF-I did not alter the PMNL surface expression of Fc gamma RI (CD64), Fc gamma RII (CDw32), or Fc gamma RIII (CD16). PMNLs exposed to IGF-I increased their f-met-leu-phe and phorbol myristate acetate-induced oxidative burst, as evaluated by hydrogen peroxide production, whereas IGF-I did not influence PMNL actin polymerization. The priming of PMNLs by IGF-I was dependent on time and concentration, and saturating amounts of a monoclonal antibody to the IGF-I receptor blocked the priming of PMNLs by this peptide. These experiments demonstrate that IGF-I can selectively stimulate mature PMNL functions, providing further evidence for the interaction between the immune and the endocrine systems.

Actins↗
PubMed1988

Adhesion-promoting receptors on phagocytes.

Phagocytes express a family of structurally related receptors, LFA-1, CR3, and p150,95, that mediate adhesion of leukocytes to a variety of cells and surfaces. LFA-1 mediates the binding of killer T cells to targets, CR3 mediates binding of phagocytes to iC3b-coated surfaces and to endothelial cells, and LFA-1, CR3, and p150,95 each mediate the binding of bacterial lipopolysaccharide. Here we review the structure and function of each of these receptors and present evidence that they are related to a larger class of adhesion-promoting receptors called integrins. Of particular emphasis are observations that the capacity of these receptors to promote adhesion is strongly and reversibly modulated by both soluble and surface-bound stimuli. We review this form of regulation and present evidence that changes in the binding activity of adhesion-promoting receptors is accomplished by changes in the two-dimensional distribution of receptors in the plane of the membrane. Inactive receptors are randomly distributed in the membrane, and their ability to bind a ligand-coated surface is enabled by a ligand-independent movement into small clusters. The implications of these structural features are discussed.

Antigens, Differentiation↗
PubMed1985

Behaviour of neutrophil leucocytes in uniform concentrations of chemotactic factors: contraction waves, cell polarity and persistence.

The essential component of any hypothesis of random or directed cell movement is the mechanism of cell polarity. In this paper we describe the polar behaviour of human neutrophil leucocytes in uniform concentrations of chemotactic factors both in suspension and while moving across surfaces. Neutrophils exposed to uniform concentrations of chemotactic factors in suspension around the dissociation constant (Kd) for the receptor rapidly become distinctly bipolar; neutrophils exposed to supraoptimal uniform concentrations (100-fold greater than Kd) of chemotactic factors in suspension, although morphologically active, never reached the same degree of polarity as cells in optimal concentrations. These differences in polarity were shown to be the direct result of equatorial contraction waves stimulated on the cell surface by interaction with chemotactic factors. In optimal concentrations of chemotactic factors, contraction waves were initiated from one region of the cell, whereas in supraoptimal concentrations of chemotactic factors contraction waves emanated from all areas of the cell surface. Asymmetry in the distribution of surface receptors for Fc and C3b were observed in neutrophils polarized in uniform concentrations of chemotactic factor. In neutrophils, motile but not well polarized (in 10(-6) M-N-formylmethionyl-leucyl-phenylalanine (fMLP), receptors were uniformly distributed. In neutrophils polarized in concentrations of fMLP near the Kd for the receptor (10(-8) M) receptors for C3b and Fc were localized in the anterior region of the moving cell. The link between contraction waves, cell polarity and receptor redistribution and their initiation by chemotactic peptides is discussed in the context of neutrophil locomotion and response to chemical signals.

Cell Movement↗
PubMed1985

Scanning electron microscopy and the study of Fc and C3b receptors of cultured fat-storing cells from rat liver.

Non-parenchymal fat-storing cells (FSCs) were isolated from rat liver by Metrizamide density centrifugation after liver perfusion with media containing pronase and/or collagenase. These cells were cultured in Williams' E medium with 20% fetal calf serum under the usual conditions. FSCs, identified by vitamin A-specific fluorescence (VAF), were viewed under conventional light microscopy 24, 48 and 72 h after seeding. At 24 h, some FSCs remained hemispheric; at 48 h all FSCs were well spread out, and at 72 h the number of FSCs had increased and the VAF intensity had become weaker. Scanning electron microscopy revealed that the features of the FSCs clearly differed from those of the other non-parenchymal cells. The in vitro FSC features closely resembled the in vivo features. FSCs cultured for 48 h had flattened, triangular or oval shapes with fairly smooth surfaces that showed scattered microvilli 0.1 micron long. Two types of processes, long slender (130 microns maximum length) and short broad ones, protruded from the cell body. These processes had smaller projections 0.2 micron wide that looked like fern leaves. Many lipid droplets could be seen under the cell surface. IgG-coated sheep erythrocytes (EAs) and IgM-C3-coated ox erythrocytes (EACs) were used to investigate whether there are Fc and C3b receptors on the FSCs. No rosette-formation characteristic of EAs or EACs was present on the FSCs; proof that FSCs have neither receptor.

Animals↗
PubMed2000

Phagocytosis and killing of Staphylococcus aureus by bovine neutrophils after priming by tumor necrosis factor-alpha and the des-arginine derivative of C5a.

OBJECTIVES: To evaluate effects of proinflammatory mediators on phagocytosis and killing of Staphylococcus aureus, the oxidative burst (OB), and expression of receptors for opsonins by bovine neutrophils. SAMPLE POPULATION: Neutrophils from 10 cattle. PROCEDURE: Neutrophils were primed with recombinant bovine tumor necrosis factor-alpha (TNF-alpha) or the des-arginine derivative of bovine C5a (C5a(desArg)) and mixed with S aureus. Phagocytosis and OB were measured by use of flow cytometry. Rate of phagocytosis and intracellular killing were evaluated. Expression of receptors for immunoglobulins and the C3bi fragment of complement were estimated by use of flow cytometry. RESULTS: Priming of neutrophils by TNF-alpha improved phagocytosis of S aureus with a concentration-dependent effect. Phagocytosis of preopsonized washed bacteria was increased by activation of neutrophils with C5a(desArg). Phagocytosis was optimal when neutrophils primed with TNF-alpha were activated with C5a(desArg). The OB of phagocytizing neutrophils was highest when TNF-alpha and C5a(desArg) were used in combination. Bactericidal activity of neutrophils was stimulated by priming with TNF-alpha or C5a(desArg). Binding of bovine IgM or IgG2 to bovine neutrophils was not stimulated byTNF-alpha, C5a(desArg), or both, and aggregated IgG1 did not bind to neutrophils regardless of their activation state. Both TNF-alpha and C5a(desArg) increased expression of beta2 integrins (CD18), with the highest expression when they were used in combination. CONCLUSIONS AND CLINICAL RELEVANCE: The mediators TNF-alpha and C5a(desArg) stimulated phagocytic killing by neutrophils and potentiated each other when used at suboptimal concentrations. Bovine neutrophils have enhanced bactericidal activities at inflammatory sites when TNF-alpha, C5a(desArg), or both are produced locally.

Animals↗
PubMed1986

Search for Fc and C3b receptors on black-eyed RCS rat RPE cells.

In the retina, the membranous outer segments shed from the photoreceptors are phagocytized by the adjacent retinal pigment epithelial cells. These cells are some of the most active phagocytic cells in the body and like photoreceptors must survive the lifetime of the organism. The initiation of engulfment by the pigment epithelial cells occurs by an unidentified mechanism. The ingestion of particles by many, but not all phagocytic cells, is mediated by Fc and C3 receptors located on the external plasma membrane. The present experiment reports our unsuccessful attempt to demonstrate either the Fc or C3b receptor on the plasma membrane of RCS rat pigment epithelial cells.

Animals↗
PubMed1989

In vitro phenotypic and functional characterization of human pigment epithelial cell lines.

We have characterized human retinal pigment epithelium (HRPE) for the expression of cell surface antigens. Primary HRPE cultures, established cell lines, and freshly brushed pigment epithelial cells all express HLA-ABC but not HLA-DR antigens. However, both primary cultures and established cell lines can be induced by gamma interferon stimulation to express HLA-DR in a dose dependent manner. Only freshly brushed HRPE cells express Fc, and no cells demonstrated the presence of C3b. Our results show that HRPE cells change in culture, as reflected by the loss of Fc receptors, but retain the ability to synthesize HLA-ABC spontaneously and HLA-DR upon stimulation.

Adolescent↗
PubMed1986

Human cord blood monocytes: binding and ingesting capacity mediated by Fc and C3b receptors.

Human cord blood monocytes have been compared to monocytes from adults. Our results show that unstimulated cord blood monocytes are as effective as monocytes from adults with regard to their binding and ingesting capacity mediated by Fc and C3b receptors. Furthermore, when stimulated with PMA (phorbol-myristate-acetate), the C3b receptor-mediated phagocytosis in cord blood monocytes was enhanced to the same extent as in monocytes from adults. These findings show that Fc and C3b receptor functions in human monocytes are fully developed at birth and cannot explain the increased susceptibility to infections seen in the neonate.

Adult↗
PubMed2000

Transfer of immune complexes from erythrocyte CR1 to mouse macrophages.

We are developing a potential therapeutic approach for removing pathogens from the circulation of primates in which the pathogen is bound to the complement receptor (CR1) on E using a bispecific mAb complex, a heteropolymer (HP). We have used mAb this approach to demonstrate that cleared prototype pathogens are localized to, phagocytosed in, and destroyed in the liver. Extension of this work to a clinical setting will require a detailed understanding of the mechanism by which the E-bound immune complex substrates are transferred to fixed tissue macrophages in the liver, the transfer reaction. Therefore, we examined an in vitro system to study this process using bacteriophage phiX174 as a model pathogen. E containing phiX174 (bound via an anti-CR1/anti-phiX174 HP) were incubated with P388D1 murine macrophages, and the two cell types were separated by centrifugation through Ficoll. Both E and macrophages were then probed and analyzed by RIA or flow cytometry. The results indicate that all three components of the E-bound IC (phiX174, HP, and CR1) were removed from the E and internalized by the macrophages. We found that transfer requires the Fc portion of IgG, because little transfer of phiX174 occurs when it is bound to E CR1 using a HP containing only Fab fragments. These findings, taken in the context of other studies, suggest a general mechanism for the transfer reaction in which Fc receptors facilitate close juxtaposition of the macrophage to the E-bound IC which then allows a macrophage-associated protease to cleave CR1. The released IC are then internalized and processed by the macrophages.

Animals↗
PubMedDate not supplied

Different transendothelial migration behaviour pattern of blood monocytes derived from patients with benign and malignant diseases of the breast.

BACKGROUND: In this study we compared the expression of selected monocyte surface antigens with the potential to transmigrate through an endothelial layer before and after surgery from breast cancer patients (CA) and patients with benign disease of the breast (BE). MATERIALS AND METHODS: Transmigration capacity of mononuclear cells was determined after isolation by Ficoll density gradient, layered over human umbilical vein endothelial cells and cultured in a two chamber plate added with fMLP as a chemotactic stimulus. We determined monocyte phenotye (HLA-DR, FcgRI/CD64, CR1/CD11b and LFA-1/CD11a) and the phagocytosis of E. coli by flow cytometry. RESULTS: Before surgery blood monocytes had an equal expression of the measured surface antigens, but were different in regard to their interaction with endothelial cells. Monocytes derived from CA had a higher transmigration potency than those of BE. Moreover, the migration through the endothelial cell layer created different populations of monocytes. Surgical stress modified transmigrated monocytes of BE into the direction of monocytes from CA. Phagocytic capacity of peripheral blood monocytes from CA was significantly diminished and was further reduced after surgery when measured in transmigrated cells. CONCLUSION: Our study shows that monocytes from CA and BE can be discriminated in regard to their interaction with endothelial cells.

Adult↗
PubMed2003

[Modulation of Fcgamma and C3b receptor expression by marine bioglycans in mouse splenocytes].

Investigation of polysacharide immunomodulators of marine origin was performed--mitilane, alpha-1,4;1,6-D-glucane, isolated from midia Crenomytilus grayanus, and translam--beta-1,3;1,6-D-glucane isolated from marine algae Laminaria cichorioides were compared. Mechanisms of phagocytes cells activation were investigated. Dose-dependent ability of investigated bioglycanes to facilitate Fc gamma R [symbol: see text] C3bR expression at mice splenocytes was demonstrated in vivo and in vitro. The effect depended on immunomodulator type, incubation conditions, dose, period of incubation in vitro and by splenocytes population used for Fc gamma R and C3bR identification. It was shown that C3bR expression was more enhanced by immunomodulators than Fc gamma R expression. For Fc gamma R induction on lymphocytes membranes the presence of phagocytes cell (macrophages and neutrophils) is obligatory. Mitilane, containing alpha-1,4;1,6-D-glucane and some amount of protein is more effective in stimulation of membrane receptors expression than translam--beta-1,3;1,6-D-glucane. The results of investigation demonstrates the possibility to use marine bioglicanes as activators of Fc gamma R and C3bR activity, that is the base for control of pathological processes, related to immune system.

Adjuvants, Immunologic↗
PubMed1992

Effects of mucoid and non-mucoid Pseudomonas aeruginosa isolates from cystic fibrosis patients on inflammatory mediator release from human polymorphonuclear granulocytes and rat mast cells.

Mucoid Pseudomonas aeruginosa causing chronic bronchopulmonary infection in cystic fibrosis (CF) patients may interfere with host defence mechanisms. We investigated 13 P. aeruginosa strains isolated from sputa of CF patients with regard to the induction or modulation of inflammatory mediator release from human neutrophils (PMN) and rat mast cells. The effects of mucoid as compared to non-mucoid bacteria were studied using a mucoid strain and its non-mucoid revertant. The release of leukotrienes (LT) and histamine in response to the majority of the CF strains was insignificant. However, preincubation of PMN with P. aeruginosa caused a dose-dependent decrease (50-95%) of LTB4 and LTC4 generation and LTB4 metabolism induced by the Ca(2+)-ionophore A23187 or opsonized zymosan (ZX) (P less than 0.001). The mucoid strains caused a three- to 10-fold higher impairment of LTB4 release (P less than 0.05) and a concomitant down-regulation of LTB4 receptors on neutrophils. Inhibitory effects were also obtained for mucoid and non-mucoid bacteria when the phorbol-ester or the Ca(2+)-ionophore induced luminol enhanced chemiluminescence response (P less than 0.001) or the histamine release from rat peritoneal mast cells (P less than 0.01) was studied. The bacteria-cell contact with non-mucoid strains was associated with an increased Ca2+ influx into PMN, whereas mucoid bacteria had no effect. In addition, a protein kinase C-dependent decrease of the C3bi receptor was suppressed by the mucoid--and less effectively--by the non-mucoid strain. The results suggest that the impairment of the phagocytic and inflammatory system may contribute to the pathogenesis and persistence of mucoid P. aeruginosa infection in CF.

Animals↗
PubMedDate not supplied

[Functional activity of phagocyte blood cells in pulmonary tuberculosis].

The characteristics of the functional activity of phagocyte blood cells in patients with destructive pulmonary tuberculosis caused by medicinal sensitive and medicinal resistant infective agents were studied. In the process of pulmonary tuberculosis, irrespective of the medicinal sensitivity of infective agents before and during treatment, a decrease in the phagocytic activity of neutrophil granulocytes and the level of the expression of Fcgamma- and C3b-receptors on monocytes with a simultaneous increase in the spontaneous production of oxygen metabolites in neutophils and a rise in the adsorptive capacity of monocytic cells were observed.

Adult↗
PubMed2006

[Peripheral blood mononuclear leucocytes in patients with drug-sensitive and drug-resistant pulmonary tuberculosis].

The authors studied functional characteristics of mononuclear leucocytes in patients with drug-sensitive and drug-resistant pulmonary tuberculosis. The study found decrease of the number of C3b- and Fcchi-receptorpositive monocytes and increase of their saturation activity in both categories of pulmonary tuberculosis before and after antituberculous therapy. The study revealed increase of interferons alpha and chi production and, at the same time, decrease of tumor necrosis factor alpha, which was more prominent in cases of drug-sensitive tuberculosis, and depression of interleukin 2 secretion, more prominent during chemotherapy in cases of drug-resistant tuberculosis.

Adult↗
PubMed1991

Phagocytosis of Mycobacterium leprae by human monocyte-derived macrophages is mediated by complement receptors CR1 (CD35), CR3 (CD11b/CD18), and CR4 (CD11c/CD18) and IFN-gamma activation inhibits complement receptor function and phagocytosis of this bacterium.

We have examined phagocytosis of Mycobacterium leprae by human monocyte-derived macrophages (MDM). Compared with monocytes, MDM exhibit greatly enhanced adherence of M. leprae (6.5 +/- 2-fold increase). MDM adherence of M. leprae is serum dependent and requires heat-labile serum components because heat inactivation of serum reduces adherence by 70 +/- 3%. mAb against C receptors CR1 (CD35), CR3 (CD11b/CD18), and CR4 (CD11c/CD18) inhibit phagocytosis of M. leprae in fresh nonimmune serum. Single mAb against each receptor inhibit M. leprae adherence by 25 +/- 4% - 33 +/- 6%. Single mAb used in combination against all three receptors inhibit M. leprae adherence by 51 +/- 6%. Most significantly, pairs of mAb used in combination against all three receptors inhibit by 80 +/- 4%. By electron microscopy, MDM ingest all M. leprae that adhere in fresh nonimmune serum. In the presence of mAb against CR1, CR3, and CR4, the percentage of MDM cross-sections that contain intracellular bacteria is reduced 66 +/- 3% and the mean number of bacteria per cross-section is reduced 78 +/- 10%. MDM activated by IFN-gamma exhibit markedly reduced adherence (by light microscopy) and ingestion (by electron microscopy) of M. leprae. MDM in culture for 5 days inhibit M. leprae adherence by 83 +/- 2% and ingestion by 88% when activated for 5 days. Paralleling this, IFN-gamma-activated MDM exhibit markedly reduced C receptor function, reflected by markedly decreased adherence and ingestion of C3b- and C3bi-coated E. Decreased C receptor function by IFN-gamma-activated MDM correlates with decreased surface expression of CR1 but not CR3 or CR4. CR1 expression on MDM in culture for 5 days is reduced by 32 +/- 9% and 75 +/- 3% after IFN-gamma activation for 5 and 2 days, respectively. This study demonstrates that MDM have an enhanced capacity to phagocytize M. leprae, and that in addition to CR1 and CR3, phagocytosis involves CR4, whose expression on MDM is highly maturation-dependent. This study also demonstrates that IFN-gamma activation markedly reduces the capacity of MDM to phagocytize M. leprae, and it provides a molecular mechanism for this phenomenon-decreased C receptor function.

Antibodies, Monoclonal↗
PubMed1991

Rapid increases in the membrane expression of neutral endopeptidase (CD10), aminopeptidase N (CD13), tyrosine phosphatase (CD45), and Fc gamma-RIII (CD16) upon stimulation of human peripheral leukocytes with human C5a.

Rapid increases in the membrane expression of C3 receptors on granulocytes and monocytes in response to the anaphylatoxin C5a have previously been described. In this study we demonstrate increases in the membrane expression of neutral endopeptidase (NEP, CD10, CALLA), aminopeptidase N (APN, CD13), tyrosine phosphatase (CD45/CD45Ro) and the Fc R Fc gamma-RIII (CD16) on granulocytes within minutes of treatment with human C5a. Monocytes responded to C5a with increases in CD13 and CD45/CD45Ro. These membrane modulations could be prevented by preincubating the C5a preparations with anti-C5a mAb C17/5 but not by pretreating the cells with cycloheximide. Increases of CD10, CD13, and CD11b but not CD11a (LFA-1) were also observed in leukocytes from patients undergoing hemodialysis with cuprophan membranes. The increase of CD16 on granulocytes was dependent on the presence of plasma during in vitro activation with C5a indicating that plasma contains inhibitors which prevent the previously described loss of Fc gamma-RIII upon stimulation of the cells.

Aminopeptidases↗
PubMed1991

Differential effects of neutrophil-activating peptide 1/IL-8 and its homologues on leukocyte adhesion and phagocytosis.

Several structural homologues of the chemotactic peptide neutrophil-activating peptide 1/IL-8 (NAP-1/IL-8) were tested for their ability to influence the expression and function of adhesion-promoting receptors on human polymorphonuclear leukocytes (PMN). NAP-2, melanoma growth stimulatory activity, and two forms of NAP-1/IL-8 (ser-NAP-1/IL-8 and ala-NAP-1/IL-8, consisting of 72 and 77 amino acids, respectively), each caused an increase in the expression of CD11b/CD18 (CR3) and CR1, which was accompanied by a decrease in the expression of leukocyte adhesion molecule-1 (LAM-1, LECAM-1). The binding activity of CD11b/CD18 was also enhanced 3- to 10-fold by these peptides, but enhanced function was transient: binding of erythrocytes coated with C3bi reached a maximum by 30 min and declined thereafter. Ser-NAP-1/IL-8, ala-NAP-1/IL-8, NAP-2, and melanoma growth stimulatory activity also caused a two- to threefold enhancement of the phagocytosis of IgG-coated erythrocytes (EIgG) by PMN without causing a large increase in the expression of Fc gamma receptors. Enhanced phagocytosis of EIgG appeared to be mediated through CD11b/CD18, because F(ab')2 fragments of an antibody directed against CD18 inhibited NAP-1/IL-8-stimulated ingestion of EIgG. The four active peptides caused a rapid, transient increase in the amount of F-actin within PMN, indicating that they are capable of influencing the structure of the microfilamentous cytoskeleton, which participates in phagocytosis. Two other NAP-1/IL-8-related peptides, platelet factor 4 and connective tissue-activating peptide III, were without effect on expression of CD11b/CD18, CR1, and LAM-1, binding activity of CD11b/CD18, or Fc-mediated phagocytosis, and increased actin polymerization only slightly. Our observations indicate that several members of the NAP-1/IL-8 family of peptides were capable of promoting integrin-mediated adhesion and Fc-mediated phagocytosis, processes important in the recruitment of PMN to sites of inflammation and antimicrobial responses of PMN.

Actins↗