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PubMed1980

Response of plasma fibronectin to major body burn.

The ability of macrophages of phagocytize particulate matter is largely dependent on fibronectin, a nonspecific opsonin found in plasma. Fibronectin depletion, resulting in reticuloendothelial system (RES) depression, occurs following a variety of physical insults. RES depression may contribute to postinjury sequelae such as respiratory distress syndrome and septicemia. Fibronectin concentration was measured in the plasma of sheep with chronic lung lymph fistulas subjected to controlled thermal injury. Fibronectin levels were significantly (p < 0.05) decreased at 4, 24, 48, and 72 hours following burning. Fibronectin concentration decreased in parallel with serum albumin concentration; serum globulin concentrations did not decrease. Fibronectin concentration had an inverse relationship to lung lymph flow, a reflection of pulmonary transvascular fluid filtration rate. The role of fibronectin in the pathogenesis of postinjury respiratory distress syndrome deserves further exploration.

Adult↗
PubMedDate not supplied

Ureaplasma urealyticum in the immunocompromised host.

The lack of antibody in hypogammaglobulinemic patients probably results in failure of mycoplasmas to be "neutralized" and accounts for the diminished ability of the patients to cope with these organisms escaping hematogenously from the respiratory and urogenital tracts. Furthermore Ureaplasma urealyticum and other mycoplasmas are ingested by neutrophils in the absence of opsonins, indicated by the fact that they are able to trigger the release of chemiluminescence from these cells; ureaplasmas are not killed during this process and it is possible that carriage occurs within phagocytes to various sites. Several mycoplasmal species have localized in joints and U. urealyticum organisms are no exception. They have been isolated from the purulent synovial fluids of at least three hypogammaglobulinemic patients in Canada, England and the United States, respectively, the arthritides responding to appropriate antibiotic therapy. In one male patient, however, repeated and prolonged episodes of arthritis over several years, associated with antibiotic-resistant ureaplasmas, responded only to the administration of specific hyperimmune serum. Apart from joint involvement subcutaneous abscesses have been seen, and in the latter patient persistent urethritis was caused by ureaplasmas, these being the only organisms recovered from the urethra. Chronic urethrocystitis/cystitis in hypogammaglobulinemic patients has been associated also with ureaplasmal infection. In addition polyarthritis with recovery of both ureaplasmas and Mycoplasma hominis from the joints has been seen in a kidney allograft patient on an immunosuppressive regimen. However, further evidence that ureaplasmas cause a problem in immunosuppressed patients or in those with the acquired immunodeficiency syndrome is lacking.

Agammaglobulinemia↗
PubMed2001

Nonopsonic phagocytosis of Pseudomonas aeruginoas: insights from an infant with leukocyte adhesion deficiency.

Children with leukocyte adhesion deficiency type I are at risk for overwhelming infection because their neutrophils lack surface beta 2 integrins (CD18/CD11) that normally interact with endothelial cell adhesion molecules and mediate migration to sites of bacterial invasion. In vitro studies of phagocytic cells from an infant with leukocyte adhesion deficiency type I demonstrated that complement receptor 3 (CD18/CD11b) mediates nonopsonic phagocytosis of some Pseudomonas aeruginosa strains and might play a control role in the control of Pseudomonas infections at sites where there are low levels of opsonins.

CD18 Antigens↗
PubMed1993

The immune system in end-stage renal disease.

Patients with end-stage renal disease present with an immunodeficient state paradoxically coexisting with signs of activation of immune system cells and that is accentuated rather than corrected by replacement dialysis therapy. The mechanisms of this immune system dysregulation presently under consideration are a reduced bioavailability of interleukin-2 secondary to its overconsumption by activated T cells; a downregulation of phagocyte adhesion molecules and opsonin receptors following their overexpression during dialysis with complement-activating membranes; an increased production of the cytokines interleukin-1, tumor necrosis factor-alpha, and interleukin-6 by activated monocytes and of soluble CD23 by B lymphocytes; and last, but far from least, the presence of uremic toxins. Perspectives of research are aimed at elucidating the respective role of the T helper cell subpopulations (Th-1 and Th-2) and the influence of the progression of chronic renal failure on the naturally occurring cytokine inhibitors, with the hope of better defining the rationale of strategies of immunomodulation that could be beneficial to patients with end-stage renal disease.

Antibody Formation↗
PubMed1988

Interaction of Bordetella pertussis virulence components with neutrophils: effect on chemiluminescence induced by a chemotactic peptide and by intact bacteria.

The effect of secreted virulence components of Bordetella pertussis on chemiluminescence (CL) of rabbit peritoneal neutrophils was determined with the chemotactic peptide N'-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) or intact B. pertussis as the stimulus. Pertussis toxin (PT) inhibited the response to fMLP in a dose-dependent manner, although only after the neutrophils had been exposed to the toxin for greater than 15 min. Both filamentous haemagglutinin (FHA) and lipopolysaccharide (LPS) markedly enhanced the CL response to fMLP after greater than or equal to 15 min incubation with the neutrophils. Similar effects to those of B. pertussis LPS were also seen with smooth and rough LPS from Salmonella minnesota. With the lowest dose of each component which elicited a maximal effect on CL, the inhibitory effect of PT overrode the enhancing effect of FHA and B. pertussis LPS. Pre-incubation of neutrophils with PT, FHA or B. pertussis LPS caused a slight reduction in the subsequent CL response to virulent B. pertussis Tohama. Virulent (phase I, or X-mode) organisms of B. pertussis 18334 and B. pertussis Tohama induced greater neutrophil CL than their avirulent (C-mode) derivatives. There appeared to be an inverse correlation between bacterial hydrophilicity and the ability to induce neutrophil CL: X-mode bacteria were significantly less hydrophilic than C-mode organisms. Three mutants, the adenylate cyclase (AC)- and haemolysin (HLY)-deficient B. pertussis BP348, the FHA-deficient B. pertussis BP353, and the PT-deficient B. pertussis BP357, generated similar levels of CL and had similar hydrophilicity values. The hydrophilicity value of the avirulent mutant B. pertussis BP347 (deficient in AC, HLY, FHA and PT) and the CL induced by this strain were similar to those of B. pertussis C-mode organisms. Thus, the interaction of B. pertussis with neutrophils appears to be complex, reflecting both the alteration of leucocyte function by secreted virulence components of the organism and, in the absence of opsonins, the surface properties of the bacterium.

Adenylate Cyclase Toxin↗
PubMed1986

Polymorphonuclear leukocytes, complement, and Trichophyton rubrum.

Trichophyton rubrum can activate complement. In order to assess the role of complement in host defense, fresh human serum was incubated with fungus. Factors were produced which were chemotactic for polymorphonuclear leukocytes (PMNL), but only if complement activation was allowed. This suggests that the chemotactic factor or factors were derived from complement. Incubation of T. rubrum with fresh serum did not prevent fungal growth on subsequent culture, but did inhibit incorporation of radiolabeled N-acetylglucosoamine. The interaction of PMNL and fungi was studied, and the role of complement as a mediator was assessed. PMNL adhered well to fungi provided that the fungal hyphae had been preincubated with fresh human serum to provide complement opsonins. Opsonized and unopsonized fungi both stimulated a respiratory burst in normal PMNL as measured by chemiluminescence, but the burst was generated much faster with opsonized hyphae. Although hyphae with adherent PMNL subsequently proliferated in culture, the incorporation of N-acetylglucosoamine was inhibited 96% when the hyphae were opsonized with fresh serum and then incubated with PMNL. Inhibition was also observed with unopsonized fungi, but to a lesser degree. Varying the ratio of PMNL to hyphae showed that inhibition by PMNL was far more efficient if hyphae were opsonized. In contrast to hyphae, opsonized fungal spores were killed by PMNL so that no growth was observed in subsequent cultures. This killing was not observed if PMNL were omitted or if spores were preincubated with heat-inactivated serum rather than fresh serum. Activation of complement apparently opsonizes the spores so that they can be ingested and killed by viable PMNL. Contents of disrupted PMNL failed to inhibit fungal growth. Complement and PMNL may aid the host in defending itself against infection by dermatophytes.

Acetylglucosamine↗
PubMed1983

Complement activation by trichophyton rubrum.

The role of complement in infections by dermatophytes is unknown. Therefore we evaluated the ability of the dermatophyte Trichophyton rubrum to activate complement in vitro. Aliquots of human plasma that had been incubated with T. rubrum were examined for evidence of complement activation. Following incubation, the total hemolytic complement activity of plasma fell 76%. Further, each T. rubrum incubation led to obvious C3 conversion and generation of polymorphonuclear leukocyte (PMN) aggregating activity. Plasma that had complement activity depleted by heat (56 degrees C x 30 min) or 10 mM EDTA failed to develop C3 conversion or PMN aggregating activity. Complement activation was not affected when the classical complement pathway was selectively blocked by MgEGTA. These studies indicate that T. rubrum can activate the complement system by the alternative pathway. The consequent generation of anaphylatoxins, chemotaxins, and opsonins might be important both in host defense against dermatophytic infections and in the inflammatory reactions mediated by them.

Animals↗
PubMed2005

Ultraviolet-B recruits mannose-binding lectin into skin from non-cutaneous sources.

Mannose-binding lectin (MBL) is an integral part of the innate immune system and functions as an opsonin by binding to pathogens and certain apoptotic cells to promote their uptake by phagocytes. We recently identified an association of low-producing MBL polymorphisms with adult dermatomyositis (DM). Our model is that MBL deficiency leads to a defect in the clearance of apoptotic debris in the skin, thereby predisposing to photosensitive autoimmune disease. In this study, we sought to determine whether MBL binds within the epidermis, and to determine its source, and potential function of this binding. We demonstrated that the MBL is present in irradiated, but not in non-irradiated skin, and in irradiated skin it is bound to apoptotic keratinocytes (KC). We found that MBL is not made by KC, showing indirectly that it comes from an exogenous source, despite the fact that other complement components are made by KC and upregulated by ultraviolet irradiation. Finally, we demonstrated that non-KC-derived MBL bound to apoptotic KC in vitro and increased the uptake of these cells by dendritic cells. We hypothesize that MBL may facilitate non-inflammatory clearance of apoptotic debris in patients with photosensitive forms of DM.

Adult↗
PubMed1988

Luminol-dependent chemiluminescence in antibody-sensitized neutrophils stimulated with protein A-bearing staphylococci.

When mouse polymorphonuclear leukocytes (PMNs) sensitized with rabbit antibody to mouse Ehrlich ascites tumor cells were stimulated by Staphylococcus aureus Cowan I cells, a conspicuous luminol-dependent chemiluminescence was observed in the absence of opsonin. The profile of the chemiluminescence (CL) response evoked by staphylococcal cells from antibody-sensitized PMNs had two peaks. An initial peak, observed within 1 min after stimulation, was sharp and high and a second peak, observed about 5 min after stimulation, was low and extended. The CL response of antibody-sensitized PMNs stimulated by S. aureus Cowan I cells was dose-dependently blocked by preincubation with soluble SpA. Cells of a mutant derived from S. aureus Cowan I strain with trace amounts of cell-bound SpA failed to stimulate the antibody-sensitized PMNs to generate the CL response. The antibody-sensitized PMNs were found to phagocytize SpA-bearing S. aureus cells even in the absence of opsonic serum. These results suggest that the observation presented here might provide a useful tool for the investigation of CL response of PMNs.

Animals↗
PubMed1989

A simple method for observation of phagocytosis on bacterial thin-layer.

A simple method was developed to visually present the phagocytic activity of leukocytes by using adherent Staphylococcus aureus cells and blood applied on a plastic dish. When heparinized blood was applied on thin-layer of heat-killed S. aureus cells on the plastic dish, plaques due to the phagocytic activity of leukocytes were observed with a microscope under a low magnification. Fewer and smaller plaques were observed when plasma-deprived rather than whole blood was used. Some analyses were made in respect to the fundamental conditions required for optimal results. This method was considered to be useful for conveniently evaluating the serum opsonin activities and phagocytic function of leukocytes in various kinds of diseases.

Antigens, Bacterial↗
PubMed1985

The 'metabolic burst' in polymorphonuclear leukocytes from patients with quiescent psoriasis.

We report an investigation of peripheral blood polymorphonuclear leukocytes (PMN) from untreated patients with mild, quiescent psoriasis. Four aspects of the 'metabolic burst' were measured to illustrate phagocytosis-related events. These were: myeloperoxidase activity, hydrogen peroxide release, superoxide production and luminol-amplified chemiluminescence. Our study does not support the concept of an intrinsic abnormality of the PMN in psoriasis, but provides additional evidence for disease activity-dependent changes in phagocytic behaviour. Possible interactions with certain humoral factors, the so-called opsonins, are discussed.

Adult↗
PubMed1994

Collectins, collectin receptors and the lectin pathway of complement activation.

The collectins are a group of soluble multimeric lectins, which contain collagenous segments, and resemble the complement protein C1q in aspects of their structures and functions. This group of proteins, which includes MBP, SP-A, SP-D, conglutinin and CL-43, are known to act as opsonins in various circumstances, and are likely to have roles in innate immunity. The focus of current research is to pursue the hypothesis that the collectins recognize and bind to non-host carbohydrate structures on microorganisms and particles, and participate in the processing or elimination of such material, either by direct interaction with phagocytic cell receptors, or by indirect routes such as complement activation .

Animals↗
PubMed1987

In-vivo studies on Haemaccel-fibronectin interaction in man.

An enzyme-linked immunoassay has been recently set up for direct measurement of the binding capacity of plasma fibronectin to gelatin. This binding capacity could be completely inhibited in vitro by an eight-fold excess of gelatin, of Haemaccel, but not of Geloplasma. On the contrary, the levels of immunoreactive fibronectin measured by laser nephelometry did not change, in presence of 10 to 1000 micrograms ml-1 of gelatin, of Haemaccel or of Geloplasma. When infused into normal volunteers, Haemaccel provoked a strong and immediate inhibition of the plasma fibronectin binding capacity to gelatin. This inhibition was dose-dependent and maximal after infusion of 500 ml of Haemaccel. Twenty-four hours after this infusion, there was a progressive recovery of the gelatin-binding capacity, which was almost completely achieved 96 h later. The formation of complexes between Haemaccel and fibronectin was demonstrated by gel filtration chromatography and by affinity chromatography. Immunoreactive plasma fibronectin levels remained unchanged up to 24 h after infusion of 500 ml of Haemaccel. A transient decline to 50% of its initial value then occurred the second day after the infusion. Therefore, a delay existed between the formation of fibronectin-Haemaccel complexes and their elimination from the bloodstream. This delay decreased when smaller volumes of Haemaccel were infused, which strongly suggests that plasma fibronectin is cleared by means of Haemaccel and does not seem to play a role of opsonin in these conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Chromatography, Affinity↗
PubMed1994

Host defence capacities of pulmonary surfactant: evidence for 'non-surfactant' functions of the surfactant system.

The most well characterized function of pulmonary surfactant is its ability to reduce surface tension at the alveolar air-liquid interface, thereby preventing lung collapse. However, several lines of evidence suggest that surfactant may also have 'non-surfactant' functions: specific components of surfactant (proteins and phospholipids) may interact with different alveolar cells, inhaled particles and micro-organisms modulating pulmonary host defence systems. SP-A, the most abundant surfactant protein, binds to alveolar macrophages via a specific surface receptor with high affinity [128]. Such binding effects the release of reactive oxygen species from resident alveolar macrophages if SP-A is properly presented to the target cell. SP-A also stimulates chemotaxis of alveolar macrophages [142], and serves as an opsonin in the phagocytosis of herpes simplex virus [161] Candida tropicalis [138] and various bacteria [137]. In addition, SP-A enhances the uptake of particles by monocytes and culture-derived macrophages [140] and improves bacterial killing. SP-D, another hydrophobic surfactant-associated protein, might interact with alveolar macrophages as well, stimulating the release of oxygen radicals [148], while for the hydrophilic surfactant proteins SP-B and SP-C no macrophage interactions have been described so far. SP-A and SP-D are members of the so-called 'collectins', pattern recognition molecules involved in first line defence. While some surfactant proteins appear to stimulate certain macrophage defence functions, surfactant phospholipids seem to inhibit those of lymphocytes. Suppressed lymphocyte functions include lymphoproliferation in response to mitogens and alloantigens, B cell immunoglobulin production and natural killer cell cytotoxicity. Concerning surfactant's phospholipid composition phosphatidylglycerol is more suppressive than phosphatidylcholine on a molar basis [38]. Bovine surfactant has an immunosuppressive effect on the development of hypersensitivity pneumonitis in a guinea pig model [150]. Despite these interesting observations, several important questions concerning the interactions of surfactant components with pulmonary host defence systems remain unanswered. Sufficient host defence in the lungs works through various humoral-cellular systems in conjunction with the specific anatomy of the airways and the gas exchange surface--how does the surfactant system fit into this network? Surfactant and alveolar cells are both altered during lung injury--is there a relationship between alveolar cells from RDS patients and the endogenous surfactant isolated from such patients? How does exogenous surfactant as used for substitution therapy modulate the defence system of the host? Some of those artificial surfactants have been shown to inhibit the endotoxin-alveolar macrophages, PMNs and monocytes including IL-1, IL-6 and TNF [139,152].(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Macrophage procoagulant activity in experimental African trypanosomiasis.

Peritoneal macrophages from mice infected with Trypanosoma brucei brucei expressed a greatly elevated procoagulant activity (PCA) which could be reversed to normal levels after trypanocidal therapy. Comparison with infection caused by the non-pathogenic T. musculi suggested that the level of PCA related to parasite pathogenicity. Unstimulated macrophages, which generate only slight PCA upon stimulation with zymosan, become hyperresponsive to this stimulus during the course of infection. Hyperresponsiveness is not a generalized feature of these cells during infection, as they become progressively hyporesponsive to the same stimulus in terms of lysosomal enzyme secretion. We were unable to demonstrate a direct role of the trypanosomes in macrophage activation; however, artificial removal of the glycoprotein coat rendered the parasites highly stimulatory for macrophages even in the absence of opsonins. These results suggest that the parasites may activate macrophages indirectly, and that the resulting elevated PCA may play a role in the abnormal blood coagulation known to occur in this disease.

Animals↗
PubMed1992

The destruction of virulent Entamoeba histolytica by activated human eosinophils.

Unlike normal (i.e., non-activated) human eosinophils that are unable to destroy virulent Entamoeba histolytica even in the presence of antibodies and complement, activated eosinophils effectively destroy the parasite in vitro without the help of opsonins, yet increase this capacity with their assistance. Many activated eosinophils succumb in the process as well, probably victims of toxic products released by dying amoebae. Human activated eosinophils thus behave more like activated macrophages than like neutrophil polymorphonuclear leucocytes that are notoriously incompetent in dealing with virulent amoebae. As a regular constituent of early inflammatory reactions, and notwithstanding the absence of blood and tissue eosinophilia in invasive amoebiasis, the activated eosinophil may play a role in the defence against E. histolytica.

Adult↗
PubMed2005

Leishmania (Viannia) braziliensis: interaction of mannose-binding lectin with surface glycoconjugates and complement activation. An antibody-independent defence mechanism.

The activation of complement on the surface of Leishmania promastigotes appears to be an important factor for parasite infectivity in the mammalian host, allowing their attachment and the invasion of macrophages via complement receptors. Mannose-binding lectin (MBL) is a well-known complement activator and an efficient opsonine. We have investigated here whether serum and purified MBL bind to and promote lysis of live promastigotes of L. braziliensis; and evaluated the deposition of MBL, C1q, C4 and C3 on the parasite surface after interaction with non-immune normal human serum (NHS). We observed that both serum MBL and the purified MBL-MASP complex bind to the surface of L. braziliensis and that this binding occurred via the carbohydrate recognition domains of MBL. The binding of MBL, however, did not affect the lytic effect of complement on the parasites. The deposition of C1q, C4, C3 and parasite lysis was observed after incubation with NHS. EDTA but not EGTA abolished C3 deposition on the parasite surface, indicating the involvement of the alternative pathway in this process. Our results indicate that MBL binds to L. braziliensis and that this is mediated by a specific carbohydrate on the surface of parasites and provides evidence for antibody-independent mechanisms that complement activation on the parasite surface.

Animals↗
PubMed1984

Fibronectin promotes binding but not ingestion of agarose beads by mouse macrophages adn human monocytes.

We have examined to what extent human fibronectin associated with agarose beads with a 5- to 10-micron diameter mediates binding and uptake of the beads by mouse macrophages and human monocytes. Native agarose beads preincubated with 125I-fibronectin were neither associated with nor taken up by mouse macrophages after 30 min of incubation under serum-free conditions. When fibronectin was cross-linked to cyanogen bromide-activated agarose beads or incubated with gelatinized beads, this resulted in a significant increase in particle binding by macrophages and monocytes as compared with gelatinized beads, whereas the fraction of cells with ingested particles remained unaltered. Native agarose beads activated by cyanogen bromide and treated with ethanolamine were to a greater extent associated with and taken up by phagocytes than fibronectin- or gelatin-coated beads. Our results indicate that fibronectin acts as an adhesive glycoprotein and not as an opsonin. Since agarose beads are activators of the alternative pathway of complement, and fibronectin is reported to bind to factor C3, we speculate that cell-derived C3b is bound to the beads and fibronectin-coated beads are ingested by the phagocytes via complement C3b receptors on the cells.

Animals↗