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At least 523 records · Page 29Linked to original sources
PubMed1985

Neutrophil specific granule deficiency.

Neutrophil specific granules are thought to be important in the evolution of the inflammatory response. Specific granules are preferentially released with minor membrane perturbation in vitro or in vivo, and secreted products probably have important effects on humoral and cellular components of inflammation. In vitro studies reveal that some secreted specific granule products activate the complement cascade to generate the chemoattractant C5a and the opsonin C3b, while other secreted products are selectively chemotactic for monocytes. Translocation of receptors for chemoattractants (fmet-leu-phe) and opsonins (C3bi) from specific granules or closely related organelles to the plasma membrane may play an important role in chemotaxis, adherence, and phagocytosis. Similar translocation of constituents of the electron transport chain involved in the respiratory burst (i.e. cytochrome b) probably plays a role in neutrophil oxidative metabolism and hydrogen peroxide generation. In vivo and in vitro studies of neutrophils from patients with congenital specific granule deficiency, acquired specific granule deficiency (thermal injury and neonates), or normal neutrophils experimentally depleted of nuclei and organelles support these conclusions. Thus, release of specific granule constituents appears to be important for amplification of the initial and subsequent phases of the inflammatory response.

Cell Aggregation↗
PubMed1995

Acute lung injury in endotoxemic pigs: role of leukotriene B4.

The role of leukotriene B4 (LTB4) in the pathogenesis of acute lung injury was examined in endotoxemic pigs. In a preliminary study, the activity and specificity of an LTB4-receptor antagonist, LY-306669, were evaluated. In vitro, LY-306669 completely blocked the functional upregulation of phagocyte opsonin receptors induced by LTB4 but had a much smaller effect on opsonin receptor upregulation induced by platelet-activating factor. In pigs treatment with LY-306669 prevented leukopenia induced by injection of authentic LTB4 but had no effect on the hematologic or hemodynamic effects of PAF or U-48816, a thromboxane-A2 mimetic. In a second study, pigs received an intravenous priming dose of lipopolysaccharide (LPS) at time (t) = -18 h and were randomized to receive 1) no further treatment (n = 5), 2) LPS (250 micrograms/kg over 1 h beginning at t = 0 h) and LY-306669 (10 mg/kg bolus and 3 mg.kg-1.h-1 infusion beginning at t = -15 min) (n = 7), or 3) LPS and vehicle (n = 6). Treatment with LY-306669 significantly ameliorated LPS-induced hypoxemia, pulmonary edema, and alveolitis. These data suggest that LTB4 is an important mediator of pulmonary dysfunction and transendothelial migration of neutrophils in LPS-induced acute lung injury.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Pulmonary bacterial clearance and alveolar macrophage function in septic shock lung.

The association between the pulmonary bacterial clearance and the development of septic shock lung has been demonstrated in porcine and canine experimental models. In order to elucidate the role of the pulmonary reticuloendothelial system in bacterial clearance, the functions of alveolar macrophages (AM) obtained by bronchopulmonary lavage were studied. Five piglets were infused intravenously with Pseudomonas aeruginosa labeled with tritiated thymidine at 3 to 6 X 10(8) CFU/kg/min. Septic shock and manifestations like those of the adult respiratory distress syndrome developed within 1 h, and the pigs died within 2 to 3 h. Pulmonary bacterial clearance was 93% initially, and progressively decreased to 29%, as Pao2 decreased and lung water increased. The number of bacteria in the serial lung biopsy specimens increased steadily, although the distribution was not homogeneous. Differential centrifugations, repeated washings, and scintillation countings of the lavage fluid showed that in vivo AM phagocytosis was nil, despite the abundant bacteria found in the lavage fluid. However, when these AM were washed and tested in vitro in the presence of optimal concentrations of opsonin and oxygen, their phagocytic capability was well preserved, and was not significantly different from that of prebacterial infusion baseline values. It is concluded that in the septic shock lung, the lung clears bacteria not primarily by AM uptake but by other mechanisms, such as mechanical leakage into the pulmonary space, or by pulmonary intravascular leukocyte uptake. The apparent AM dysfunction in vivo is not intrinsic, and is likely to be caused by microenvironmental factors, such as lack of adequate opsonin and oxygen.

Animals↗
PubMed2000

Surfactant protein-A enhances uptake of respiratory syncytial virus by monocytes and U937 macrophages.

Surfactant protein (SP)-A is a known opsonin for a variety of pulmonary pathogens. SP-A enhances ingestion of these pathogens by interaction with an SP-A receptor (SP-AR) found on phagocytic cells such as peripheral blood monocytes (PBMC) and alveolar macrophages. Respiratory syncytial virus (RSV) is the most important respiratory pathogen in children. Recent studies have indicated that SP-A levels may be decreased in RSV bronchiolitis and pneumonia. In this study we examined the role of SP-A in uptake of RSV by both PBMC and U937 macrophages, a human macrophage cell line known to express SP-ARs. In addition, we studied the effect of SP-A- mediated uptake of RSV on production of tumor necrosis factor (TNF)-alpha and interleukin (IL)-10 by these cells because incomplete immunity to recurrent RSV infection has been partially attributed to abnormal cytokine responses by macrophages. SP-A enhanced binding and uptake of fluorescently labeled RSV (RSV-FITC) by PBMC in a dose-dependent manner, with a maximal effect seen with 10 to 15 microg/ml SP-A as measured by both percent fluorescent monocytes and linear mean fluorescence (lmf) of individual cells. SP-A also enhanced uptake of RSV-FITC by U937 macrophages, with a maximal effect seen with 20 microg/ml SP-A as measured by both percent fluorescent monocytes and lmf. With respect to TNF-alpha levels, RSV alone slightly enhanced TNF-alpha production by PBMC and decreased TNF-alpha production by U937 macrophages measured at 12 h after addition of RSV. SP-A-mediated uptake of RSV significantly enhanced TNF-alpha production by PBMC and reversed the RSV-induced depression of TNF-alpha by U937 macrophages. RSV significantly enhanced IL-10 production by both cell types, which was reversed by SP-A-mediated uptake. These findings suggest that SP-A is an important opsonin for RSV and that SP-A-mediated uptake of RSV may alter some of the unusual cytokine responses that are postulated to be involved in incomplete immunity to recurrent infection.

Humans↗
PubMed2000

Modulation of alveolar macrophage phagocytosis by leukotrienes is Fc receptor-mediated and protein kinase C-dependent.

We have previously established an important role for leukotrienes (LTs) in augmenting rat alveolar macrophage (AM) phagocytosis of Klebsiella pneumoniae opsonized with complete immune serum (IS), which contains the two well-known opsonins, immunoglobulin (Ig) G and complement (C). In this report, the specific opsonin requirements for LT modulation of AM phagocytosis and the dependence of this response on protein kinase (PK) C activity were investigated. Phagocytosis of K. pneumoniae opsonized with IS, non-immune serum, or heat-inactivated immune serum and of inert targets (IgG-opsonized fluorescent microspheres or C-opsonized sheep red blood cells) was examined. Inhibition of endogenous LT synthesis or action attenuated, whereas the addition of exogenous LTs augmented, phagocytosis only of targets opsonized with IgG. LTs had no effect on phagocytosis of C-opsonized or unopsonized targets. LTs did not affect adherence of IgG-opsonized targets, implying instead an enhancement of internalization. Macrophage internalization of phagocytic targets has previously been shown to require PKC activity. Pretreatment of AMs with the PKC inhibitors staurosporine or calphostin C, or with phorbol 12-myristate 13-acetate to deplete PKC, completely inhibited the ability of LTB(4) and largely inhibited the ability of LTC(4) to augment phagocytosis of IgG-opsonized microspheres. These results demonstrate that LT enhancement is confined to Fc receptor (FcR)-mediated phagocytosis. Moreover, PKC activation represents an important mechanism by which LTs promote FcR-mediated phagocytosis.

Acetophenones↗
PubMed1982

Human alveolar macrophage cytophilic immunoglobulin G-mediated phagocytosis of protein A-positive staphylococci.

Human alveolar macrophages (AM) have recently been reported to ingest and kill a strain of Staphylococcus (502A) in the absence of opsonins. To further investigate the mechanism of non-opsonic recognition, we studied phagocytosis of 23 clinical and laboratory strains of S. aureus and Staphylococcus epidermidis by AM, and by blood polymorphonuclear leukocytes (PMN) and monocytes (MN). In the absence of opsonins, AM phagocytized 18 protein A-positive but not 5 protein A-negative strains of staphylococci, and the efficiency of phagocytosis directly correlated with the amount of protein A present in the bacterial cell wall (r = 0.86, P less than 0.001). Furthermore, AM rosetted around protein A-coated Sepharose beads, but not around beads without protein A. In contrast, PMN did not phagocytize nonopsonized staphylococci, and did not rosette around either type of Sepharose. MN phagocytized protein A-positive staphylococci, but much less efficiently than AM, and showed some rosetting around protein A-coated Sepharose. The nature of the AM receptor for protein A-positive staphylococci was studied. The surface of AM was positively stained with fluorescein-conjugated antibody to human IgG, but not with IgA- or IgM-specific conjugates. No such surface-immunoglobulins were detected on PMN, and MN were only weakly positive for surface IgG. Pretreatment of AM with F(ab')2 fragments specific for human IgG (anti-Fc) inhibited subsequent phagocytosis of protein A-positive staphylococci. There was no evidence that the AM surface IgG was aggregated or immunecomplexed. From these studies we conclude that human AM possess cytophilic IgG antibodies, which can function as receptors for phagocytosis of protein A-positive staphylococci.

Animals↗
PubMed1990

The immunoglobulin G subclass composition of immune complexes in cystic fibrosis. Implications for the pathogenesis of the Pseudomonas lung lesion.

It has been shown that pulmonary macrophage (PM) phagocytosis of Pseudomonas aeruginosa (PA) is inhibited in the presence of serum from cystic fibrosis (CF) patients colonized by Pseudomonas, and that these sera contain high concentrations of IgG2 antibodies. The goal of these studies was to investigate the role that IgG2-containing immune complexes (IC) play in this inhibition of both PM and neutrophil phagocytosis. We found that serum IgG2 concentrations were elevated significantly in CF patients with chronic PA colonization and that in selected sera from CF patients with chronic PA colonization (CF + IC, n = 10), the mean IC level was significantly elevated (2.90 +/- 0.22 mg/dl [SEM]). IgG2 comprised 74.5% of IgG precipitated in IC from CF + IC sera. An invitro phagocytic assay of [14C]PA uptake using CF + IC whole-sera opsonins confirmed that endocytosis by normal PM and neutrophils was significantly depressed. Removal of IC from CF + IC sera resulted in significantly decreased serum IgG2 concentrations without a significant change in the other subclass concentrations, and enhanced [14C]PA uptake by PM (26.6% uptake increased to 47.3%) and neutrophils (16.9% increased to 52.6%). Return of the soluble IgG2 IC to the original CF sera supernatants and the positive control sera resulted in return of the inhibitory capacity of the CF + IC sera. We conclude that immune sera from patients with chronic Pseudomonas infections characterized by elevated IgG2 subclass level functions poorly as an opsonin. In these individuals, IgG2 contributes significantly to circulating IC and removal of IC, matched by a simultaneous fall in IgG2, improves bacterial uptake by neutrophil and mononuclear phagocytes. IgG2 antibodies exert antiphagocytic effects by both direct inhibition and the formation of IC.

Adult↗
PubMed2006

The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells.

Pentraxins (PTX) and complement belong to the humoral arm of the innate immune system and have essential functions in immune defense to microbes and in scavenging cellular debris. The prototypic long PTX, PTX3, and the first component of the classical complement pathway, C1q, are innate opsonins involved in the disposal of dying cells by phagocytes. Whether the interaction between various innate opsonins impacts on their function is not fully understood. We show here that characterized Toll-like receptor (TLR) ligands elicit the production of C1q and PTX3 by immature dendritic cells (DC). Moreover, these molecules bind to dying cells with similar kinetics, although they recognize different domains on the cell membranes. PTX3 binds in the fluid phase to C1q, decreasing C1q deposition and subsequent complement activation on apoptotic cells. C1q increases the phagocytosis of apoptotic cells by DC and the release of interleukin-12 in the presence of TLR4 ligands and apoptotic cells; PTX3 inhibits both events. Moreover, PTX3 inhibited the cross-presentation of the MELAN-A/melanoma antigen-reactive T cell 1 (MART-1) tumor antigen expressed by dying cells, even in the presence of C1q. These results suggest that interaction of C1q and PTX3 influences the clearance of apoptotic cells by DC. The coordinated induction by primary, proinflammatory signals of C1q and PTX3 and their reciprocal regulation during inflammation influences the clearance of apoptotic cells by antigen-presenting cells and possibly plays a role in immune homeostasis.

Antigen Presentation↗
PubMed2001

Receptors for unopsonized particles: the role of alveolar macrophage scavenger receptors.

The lung is constantly exposed to potentially pathogenic particles and microorganisms. Alveolar macrophage (AM) binding of inhaled environmental particles is a critical first step in phagocytosis and clearance, and must be accomplished without the benefit of opsonization by specific antibodies. Opsonin-independent phagocytosis is initiated by direct recognition of phagocytic target. The identities of receptors on AMs that mediate unopsonized particle binding were, until recently, not known. Using flow cytometry, monoclonal antibody and expression cloning techniques we have found a major role for the scavenger receptor, MARCO in AM binding of particles and bacteria. In this review we will discuss the role of scavenger receptors in AM binding of unopsonized particles and the use of flow cytomety in analyzing AM-particle interaction. We will also discuss other non-scavenger receptors involved in opsonin-independent phagocytosis.

Animals↗
PubMedDate not supplied

Modulation of IgG and complement receptor expression of phagocytes in kidney cancer patients during treatment with interferon-alpha.

BACKGROUND: The mode of action of interferon involves both direct cytotoxic and antiproliferative effects on the tumour cell and indirect effects that facilitate immune detection by the host. Among the immunological effects of interferon-alpha is the activation of monocytes. As opsonin receptors are crucial in the function of phagocytes, e.g. monocytes and neutrophils, their modulation by interferon-alpha (INF-alpha) merit to be further clarified. We hypothesised that the role of phagocytes in defence against cancer is reflected in the expression of opsonin receptors for IgG and complement, which further could be modified by INF-alpha. PATIENTS AND METHODS: The expression of the receptors for IgG and complement was studied in neutrophils and monocytes from blood samples of 18 kidney cancer patients treated with INF-alpha and from 39 healthy individuals. Blood samples were collected prior/to and during treatment with INF-alpha, 4.5 to 13.5 MU t.d.w., subcutaneously. After lysing the red blood cells, the samples were incubated with fluorochrome conjugated monoclonal antibodies specific for IgG (Fc gammaRI, -RII and -RIII) and complement (CR1, CR3) receptors and then analysed in flow cytometry. The results were given as the mean log fluorescence intensity (a measure of receptor number) and as the proportion of receptor-positive cells. In the in vitro experiments, the direct effect of interferon-alpha on the receptors of neutrophils and monocytes was studied. RESULTS: In patients before any treatment, the expression of CR3 and Fc gammaRI receptors in neutrophils and all receptors except Fc gammaRIII in monocytes was significantly raised when compared to the controls. Treatment with INF-alpha, induced statistically significant; transient changes in CR1-receptor expression in neutrophils and Fc gammaRI expression in monocytes. Incubation of blood cells with INF-alpha in vitro confirmed the induction of CR1 receptors in neutrophils. CONCLUSION: Changes in receptor expression reflect the inflammatory activation of phagocytes in metastatic kidney cancer. The pattern of receptor expression differs from that observed in infectious diseases. Interferon-alpha both in vivo and in vitro modulates the expression of phagocytic receptors.

Aged↗
PubMed1992

The killing of Entamoeba histolytica by activated human eosinophils.

Unlike normal, opsonin aided human eosinophils, fMLP-activated human eosinophils are capable of destroying virulent E. histolytica. Opsonins are not required for this action, although they enhance the effect. Some activated eosinophils succumb in the action as well, probably victims of toxic products released by dying amebas. Activated eosinophils thus appear to resemble activated macrophages in their dealing with this parasite.

Adult↗
PubMed2004

[The mast cells phagocytose bacteria].

In the last years there has been a growing number of reports concerning the role of mast cells in host defense against bacteria. The mast cell membrane is replete with many receptors/molecules, including those that promote the recognition and binding of bacteria. Mast cells exhibit two basic mechanisms of microbial recognition: opsonin-dependent (via Fc and C3 receptors) and opsonin-independent (via integrins, CD48 molecule and Toll-like receptors). Moreover, mast cells phagocytose and kill adherent bacteria. Phagocytosis of bacteria results in the presentation of bacterial antigens for MHC class I to T cells.

Animals↗
PubMed1977

Analysis of antibody response and immunoglobulins in sera of rabbits and guinea pigs immunized with Coxiella burnetii.

Rabbit and guinea pig sera and their immunoglobulin fractions (IgM and IgG) were examined by complement-fixation (CF), microagglutination (MA), opsonization-phagocytosis (OP) and serum protection (SP) tests at intervals after immunization with live phase I and phase II Coxiella burnetii suspensions. In general, MA antibodies, but also decreased, earlier than CF antibodies. The anamnestic immune response was higher with lower primary doses. Both phase II and phase I CF and MA antibodies as well as phase I opsonins and protective antibodies were found in either immunoglobulin fraction depending on post-immunization intervals. At later intervals and especially after the second immunizing dose the levels of protective antibodies in whole sera, but mainly in the IgG fractions, showed a better agreement with those of phase I opsonins rather than of phase I CF and MA antibodies.

Agglutination Tests↗
PubMed1990

[Fibronectin and its clinical significance in patients with osteoarthrosis, psoriatic arthropathy and chronic prostatis with a joint syndrome].

The differential diagnostic importance of plasma fibronectin in rheumatology is still undecided. Its role as opsonin is being discussed at present. The fibronectin plasma level is discussed in relation to the severity of the disease, characterized by morphologic and quantitative radionuclide indices, in 30 patients with osteoarthrosis, 10 patients with psoriatic arthropathy, 32 patients with chronic urethroprostatitis and joint syndrome and in 34 healthy controls. The results for plasma fibronectin (controls--382.0 +/- 91.0, osteoarthrosis I stage--266.0 +/- 40.1, osteoarthrosis II stage--400.6 +/- 38.7, osteoarthrosis III stage--550.7 +/- 48.2, psoriatic arthropathy I stage--322.6 +/- 35.3, psoriatic arthropathy II stage--443.3 +/- 41.4, psoriatic arthropathy III stage--471.5 +/- 36.7, chronic bacterial prostatitis--287.6 +/- 86.0, non-bacterial prostatitis--360.0 +/- 83.8, chronic trichomonas prostatitis--447.6 +/- 67.0 g/ml) are reliable supplement which characterized the destructive--reparative joint reaction and the features of the joint syndrome in chronic urethroprostatitis which takes place in opsonin deficit.

Adult↗
PubMed1989

[Treatment of endotoxin shock due to gram-negative bacteremia using extracorporeal circulation].

The effectiveness and significance of the various therapeutic methods of extracorporeal circulation were assessed in an experimental model of septic endotoxin shock. After sepsis was produced in 30 puppies by intravenously injecting 5 X 10(9) CFU/ml/kg of E. coli, on-line plasma exchange, conventional plasma exchange, charcoal plasma perfusion, hemofiltration, and sham perfusion were performed for 2 hr. As a result, 4 of the 5 puppies in the on-line plasma exchange group and one of the 5 in the conventional plasma exchange group survived; the others all died. In the on-line plasma exchange group, the number of E. coli decreased to 2.5 X 10 CFU/ml at the end of the treatment, while it was 1.3 X 10(3) CFU/ml in the sham perfusion group. The endotoxin concentration was also reduced significantly, while plasma opsonin activity was remarkably elevated. These results suggest the significance of achieving the elimination of endotoxin in blood and an increase in plasma opsonin activity simultaneously in the treatment of septic endotoxin shock.

Animals↗
PubMed1978

[Immunologic examination after posttraumatic splenectomy in childhood (author's transl)].

Immunologic examination was done in 26 patients on to 20 years after posttraumatic splenectomy at the age of 3 to 6 years of life. Immunologic parameters used were: concentration of IgG, IgA, IgM, isoagglutinins, heterophila antibodies, agglutinins against staphylococci E. coli and pertussis, serum opsonins for E. coli and pneumococci, serum haemolytic complement activity, C3C4, B- and T- subpopulations of lymphocytes, inhibition migration of mononnuclear cells with E. coli. Pathologic susceptibility to infections was not observed clinically. IgM, E. coli agglutinins and E. coli opsonins were significantly lower in the postsplenectomy group than in controls.

Abdominal Injuries↗
PubMed1988

Potential roles of fibronectin in cutaneous wound repair.

Fibronectin has many potential roles in wound repair, including chemotactic factor activity for monocytes, fibroblasts, and endothelial cells; opsonin activity and opsonin promoter activity for microorganism and tissue debris; substratum for cell migration and localization; and a scaffold for building extracellular matrix. Although fibronectin has been reported to have intrinsic growth-promoting ability, coisolation of authentic growth factors with fibronectin raises doubts about this observation. Whether the addition of exogenous fibronectin to wounds can augment healing is a question for future studies.

Acute-Phase Reaction↗
PubMed1988

Pulmonary host defense: defects that lead to chronic inflammation of the airway.

Current knowledge of pulmonary host defense can help us to understand the unique relationship between CF patients and P. aeruginosa colonization of the lung. Subtle defects in CF host defense, such as those identified in mucociliary clearance and in the CF IgG opsonin, allow P. aeruginosa to persist. Not all the defects are attributable to the host. In several examples, the defects are induced by P. aeruginosa, presumably in an effort to maintain its foothold. The examples of the latter discussed here have included the effect of pseudomonas-derived products on mucociliary action, alpha 1 PI function, and the formation of ineffective IgG opsonins and immune complexes. Overall, P. aeruginosa is the cause of significant morbidity and, eventually, mortality in these patients. As we approach the identification of the genetic defect central to this disease, it is hoped that we will gain more insight into the pathogenesis of the P. aeruginosa lung lesion in CF and develop more effective ways of preventing P. aeruginosa colonization of the CF patients' lungs.

Bronchitis↗