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At least 829 records · Page 46Linked to original sources
PubMed1998

Bovine lactoferrin stimulates the phagocytic activity of human neutrophils: identification of its active domain.

Bovine LF (bLF) at concentrations in the range of 50-250 micrograms/ml enhanced the phagocytic activity of human neutrophils as determined by measuring the incorporation of FITC-labeled latex beads by flow cytometry. The stimulatory effect of bLF was not abrogated by hydrolysis with pepsin. Bovine lactoferricin (bLFcin), which is a bactericidal fragment purified from a pepsin hydrolysate of bLF (bLFH), also enhanced the phagocytic activity, whereas, in contrast, the fraction of bLFH depleted of bLFcin showed no stimulatory effect. The phagocytosis-enhancing activity of bLF still remained after washing the neutrophils, following exposure to bLF. Also, bLF pretreatment of the latex beads stimulated their uptake. These results demonstrate that bLF is effective in promoting the phagocytic activity of human neutrophils. This activity appears to be due to its bLFcin domain and may involve dual mechanisms of direct binding to neutrophils and opsonin-like activity.

Animals↗
PubMed1999

Increased complement biosynthesis by microglia and complement activation on neurons in Huntington's disease.

In this study complement activation and biosynthesis have been analysed in the brains of Huntington's disease (HD) (n = 9) and normal (n = 3) individuals. In HD striatum, neurons, myelin and astrocytes were strongly stained with antibodies to C1q, C4, C3, iC3b-neoepitope and C9-neoepitope. In contrast, no staining for complement components was found in the normal striatum. Marked astrogliosis and microgliosis were observed in all HD caudate and the internal capsule samples but not in normal brain. RT-PCR analysis and in-situ hybridisation were carried out to determine whether complement was synthesised locally by activated glial cells. By RT-PCR, we found that complement activators of the classical pathway C1q C chain, C1r, C4, C3, as well as the complement regulators, C1 inhibitor, clusterin, MCP, DAF, CD59, were all expressed constitutively and at much higher level in HD brains compared to normal brain. Complement anaphylatoxin receptor mRNAs (C5a receptor and C3a receptor) were strongly expressed in HD caudate. In general, we found that the level of complement mRNA in normal control brains was from 2 to 5 fold lower compared to HD striatum. Using in-situ hybridisation, we confirmed that C3 mRNA and C9 mRNA were expressed by reactive microglia in HD internal capsule. We propose that complement produced locally by reactive microglia is activated on the membranes of neurons, contributing to neuronal necrosis but also to proinflammatory activities. Complement opsonins (iC3b) and anaphylatoxins (C3a, C5a) may be involved in the recruitment and stimulation of glial cells and phagocytes bearing specific complement receptors.

Adult↗
PubMed2002

Serum amyloid P component and C-reactive protein opsonize apoptotic cells for phagocytosis through Fcgamma receptors.

Serum amyloid P component (SAP) and C-reactive protein (CRP) are opsonins that react with nuclear autoantigens targeted in systemic autoimmunity. CRP and SAP bind to apoptotic and necrotic cells, which are potential sources of these autoantigens. We have recently determined that the receptors for CRP on phagocytic cells are Fcgamma receptors. The goal of this study was to determine whether CRP and SAP promote phagocytosis of apoptotic cells and to identify the receptors involved. Apoptosis was induced in human neutrophils (PMN) and the Jurkat T-cell line by UV-irradiation. SAP treatment of apoptotic human PMN increased ingestion by autologous macrophages. Both SAP and CRP increased ingestion of apoptotic, but not normal Jurkat cells by J-774 macrophages and mouse peritoneal macrophages. Neither SAP nor CRP increased ingestion of apoptotic Jurkat cells by macrophages from FcR gamma-chain deficient mice, which lack FcgammaRI and FcgammaRIII. Inhibition of FcgammaRIII-mediated uptake using mAb 2.4G2 eliminated opsonization by SAP, but not by CRP. These results indicate that pentraxins promote uptake of apoptotic cells through FcgammaRI and/or FcgammaRIII. Ingestion through these receptors is expected to alter the pattern of cytokine production and antigen presentation in response to apoptotic cells.

Animals↗
PubMed1997

A Film Tension Theory of Phagocytosis

A film tension criterion is derived on the basis of which it is possible to evaluate the probability of a particle or vesicle being phagocytosed by phagocytic cells. Variations of this criterion are arrived at by mechanical and thermodynamical analyses. Specific receptor-ligand binding interactions are included in the analysis, as are electrostatic, steric repulsive, and van der Waals attractive interactions between the surface of the phagocytosed particle and the pseudopods of the host cell membrane. Cytoskeletal forces proximate to the membrane are also implicitly included in the approach. The film tension criterion is shown to reduce to the classical wettability criterion in the limit of purely passive phagocytosis, wherein there are no electrostatic, steric repulsive, or receptor-ligand binding interactions between the cell and the phagocytosed particle. Several formulas characterizing various aspects of phagocytosis are derived. Opsonized particles are demonstrated to be more readily phagocytosed than nonopsonized particles, owing both to the energy of specific binding between opsonins and cell receptors and to the lowering of membrane tension that occurs in the vicinity of spreading pseudopods as a result of spontaneous actin polymerization. It is shown that certain particles or vesicles (those that are most easily phagocytosed) tend to be ingested more readily with increasing particle size, while others (those less easily phagocytosed) tend to be ingested more readily with decreasing size. In the limit of purely passive phagocytosis, formulas are developed for predicting the relative volumetric and particle-number uptake by cells as a function of organic/water partition coefficients. Partition coefficients of polystyrene particles and polymerized liposomes were measured and used to make theoretical predictions of particle uptake by macrophages. These predictions are compared with phagocytic uptake data for hydrophilic and hydrophobic nano- and microparticles. The comparisons show agreement between predicted trends of volumetric and particle-number uptake as a function of particle size, with uptake of hydrophilic nanoparticles diminishing with increasing size and uptake of hydrophobic nanoparticles increasing with increasing size (at least for submicrometer particles that are relatively insensitive to gravitational forces). Additional comparisons between published experimental data and theoretical predictions are also made. The potential use of the theory in characterizing the tendency of drug-loaded polymeric particles to be engulfed by macrophages is emphasized.

Journal Article↗
PubMed1997

Phenotypic variants of meningococci and their potential in phagocytic interactions: the influence of opacity proteins, pili, PilC and surface sialic acids.

In previous studies we have examined the roles of meningococcal surface structures (capsule, lipopolysaccharides, pili and opacity proteins: Opa and Opc) in bacterial interactions with human epithelial, endothelial and mononuclear phagocytic cells. In the current investigations, using defined derivatives of a serogroup A strain C751 and a serogroup B strain MC58, we studied the roles of these structures with human polymorphonuclear phagocytes (PMN). In addition, we examined the potential influence of the pilus-associated protein, PilC, previously known to affect epithelial cell interactions. The data show, that, as with monocytes, opacity proteins affect bacterial interactions with PMN and require surface sialic acids (on capsule and LPS) to be down-modulated in order to function. Also, in contrast to their role in human epithelial and endothelial adherence, neither pili nor PilC expression had any effect on phagocytic cell interactions with respect to induction of chemiluminescence as well as phagocytic killing. Examination of the relative influence of Opa and Opc indicated that Opa proteins are more effective than Opc in PMN interactions whereas the reverse was the case with monocytes. These results suggest that Opa and Opc mediate interactions with phagocytic cells via distinct mechanisms. Observations presented here and reported previously collectively show that the structural requirements of meningococci for interacting with phagocytes, in the absence of opsonins, are present in the phenotype which is often isolated from the nasopharynx (asialylated, piliated, Opa/Opc+) whereas the phenotype prevalent in the blood (sialyted, piliated, Opa/Opc+) retains the ability to adhere to endothelial cells (via pili) but appears to be refractory to interactions with phagocytic cells.

Antigens, Surface↗
PubMed1997

Lipopolysaccharide binding protein from normal human plasma purified with high efficiency.

Lipopolysaccharide (LPS)-binding protein (LBP) is an acute-phase plasma glycoprotein of 60 kDa which functions as an opsonin on activation of macrophages by bacterial LPS. The importance of LBP on the host defense against infection has been demonstrated. Human LBP has been purified from ascitic fluid or acute-phase serum. However, clinical samples often are not available, so we developed a method to purify LBP from normal plasma. The purification was accomplished by barium citrate precipitation, followed by three-step ion-exchange chromatography. The final step was Mono S cation-exchange chromatography, following Bio-Rex 70 and Mono Q chromatography, and it enabled the specific activity to increase overall 48,000-fold. This seems to be the first report of the use of Mono S column to purify LBP. The LBP obtained using these steps proved to be homogeneous by SDS-PAGE, Western blotting, and N-terminal sequence and amino acid composition analyses. The purification method established here will compensate when normal plasma with a low LBP content is available as the starting source.

Acute-Phase Proteins↗
PubMed1992

[The effect of taurolin on endogenous immunity and pathogen elimination in human peritonitis].

The influence of taurolin on phagocytosis-related defense functions and on the elimination of bacteria has been investigated in a controlled study. Particle opsonisation, a prerequisite for sufficient phagocytosis, was undisturbed in presence of up to 0.1% taurolin. Intraabdominal taurolin application did not diminish the leukocyte influx into the abdominal cavity. Opsonic capacity of peritoneal exudate was low in the taurolin group. These exudates contained more severe bacterial contamination, suggesting that this deficit was due to enhanced specific consumption of opsonins. Taurolin treatment resulted in a marked reduction of bacterial growth. Thus the substance provides antiseptic capacities without afflicting the physiological defense systems.

Aged↗
PubMed1979

Host-parasite relationship in staphylococcal infections: the role of the staphylococcal cell wall during the process of phagocytosis.

Evidence is presented that antibodies against staphylococcal peptidoglycan are important opsonins for phagocytosis of staphylococci. Cell wall protein A inhibits opsonization by IgG through its interaction with the Fc fragment of the IgG molecule and preventing therefore the binding between the Fc fragment and the Fc receptor of the cell membrane of the leukocyte. Extracellular protein A interferes with opsonization presumably through depletion of complement.

Antibodies, Bacterial↗
PubMed1981

Clearance and killing of Candida albicans in the perfused mouse liver.

Hepatic interactions of C. albicans with perfused mouse livers were characterized and compared in normal and glucan-treated mice. Normal livers, in the absence of serum, trapped greater than 90% and killed greater than 20% of the infused yeast. Phenylbutazone had no effect. Silica treatment abolished killing and decreased trapping suggesting that candidicidal activity of the liver is mediated by Kupffer cells. Immune serum, but not normal serum, enhanced trapping and killing in normal livers. Liver hypertrophy was evident in mice treated with glucan, but no enhanced candidicidal activity was observed in the absence of humoral factors. Specific immune serum and normal serum increased killing of C. albicans in glucan stimulated liver, suggesting a requirement for serum opsonin in facilitating glucan enhanced killing. Specific immune serum potentiated the greatest increase in killing. Glucan treatment in conjunction with immune serum increased killing to approximately 40%. D-mannose, but not D-glucose or D-mannitol impaired trapping of the yeast in livers of normal mice. Together, the data suggest that hepatic trapping of C. albicans involves phagocytic events as well as interactions of the yeast with surface receptors on sinusoidal cells and support the role for the liver in restricting hematogenous dissemination of C. albicans in the infected host.

Animals↗
PubMed1985

Plasma fibronectin concentrations in healthy and septic infants.

The concentration of plasma fibronectin was determined by Laurell's electroimmunoassay in 75 preterm or term newborns within the first 2 days of life, in 97 healthy infants aged from 3 days to 12 months, in 40 septic infants and in 38 healthy adult subjects. The mean fibronectin concentration in citrated plasma of normal adults was 318 +/- 84 ml/l. Healthy eutrophic term newborns 1-2 days old had approximately one-third of the fibronectin concentration of adults. There was no significant difference in the values between healthy term and eutrophic preterm newborns or between eutrophic and hypotrophic newborns. The plasma fibronectin increased strongly over the 1st month of life. No significant difference was observed between fibronectin levels in infant boys and girls. The values in septic newborns and septic older infants were significantly lower when compared with those of age-matched healthy controls. It is speculated that this deficiency, because of linkage to fibrin in disseminated intravascular coagulation or due to increased utilisation as a nonspecific opsonin and sequestration at sites of tissue injury, may contribute to organ failure in septicaemia.

Adult↗
PubMed1988

Exudate polymorphonuclear leukocytes isolated from skin chambers are primed for enhanced response to subsequent stimulation with chemoattractant f-Met-Leu-Phe and C3-opsonized yeast particles.

The ability to respond metabolically to stimulation with both soluble and particulate substances was investigated in human polymorphonuclear leukocytes (PMNLs) isolated from an aseptic inflammatory reaction. Exudate PMNLs isolated from skin chambers (E-PMNLs) and blood PMNLs isolated from the peripheral blood (B-PMNLs) of the same individual were investigated in parallel. E-PMNLs were primed, resulting in an increased chemiluminescence (CL) response to subsequent stimulation with the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (FMLP) (334%) and serum-opsonized yeast particles (C3 yeast) (201%), as compared to B-PMNLs. Phorbol myristate acetate (PMA) on the other hand, induced a CL response in E-PMNLs that was only 70% of the response obtained in B-PMNLs. A similar primed state resulting in enhancement of the CL response to FMLP and C3 yeast could be induced in B-PMNLs by pretreatment with a bacterial culture filtrate. Pretreatment of E-PMNLs with the bacterial culture filtrate, however, did not increase the CL response to FMLPs any further. The enhanced functional response to FMLPs in E-PMNLs was accompanied by an increased binding of the peptide, demonstrated by a doubling of the amount of bound f-Met-Leu-[3H]Phe (209%), as compared to B-PMNLs. The increased C3-yeast-induced CL generation in E-PMNLs was accompanied by an increased ingestion and attachment of C3-opsonized yeast particles. The enhancement of phagocytosis in E-PMNLs was, however, dependent upon the opsonin used, since IgG-opsonized yeast particles were phagocytosed to the same extent by E-PMNLs and B-PMNLs, thereby indicating that selective receptor modulation is also involved in the priming of E-PMNLs for an enhanced response to C3-yeast. These results show that exudate cells isolated from skin chambers are modulated with respect to receptor-mediated functions resulting in an increased metabolic response to FMLP coupled with an increased binding of the peptide and an increased phagocytosis of C3-coated yeast particles. Receptor modulation during exudation may be an important mechanism in regulating the inflammatory response by PMNLs.

Chemotaxis, Leukocyte↗
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↗
PubMed1976

Defects in granulocyte function in various chromosome abnormalities (Down's-, Edwards'-, Cri-du-chat syndrome).

In five infants with autosomal aberrations and diminished resistance to infection (in spite of intact humoral and cellular immune mechanisms) several granulocyte functions (chemotaxis, phagocytosis, intracellular killing and metabolism of killing) were measured. A serum-dependent or a cell-dependent disturbance of phagocytosis of Candida albicans was found in two infants with cat-cry syndrome and one with trisomy 18. In one of these children there was an additional serum dependent defect of the killing of Candida albicans and of Staphylococcus aureus, serum levels of opsonins (IgG, IgM, CH50 and C3) being within normal range. An infant with trisomy 21 showed, in addition to a cellular defect of chemotaxis, a reduced cellular ability of the killing of Staphylococcus aureus and of Escherichia coli in autologous and AB-pool-serum. Phagocytosis of these bacteria remained normal.

Blood Bactericidal Activity↗
PubMed1988

The role of staphylococcal lectins in human granulocyte stimulation.

The anti-staphylococcal activity spectrum of human polymorphonuclear leucocytes (PMN) is widely ranged. Using chemiluminescence measurements, the opsonin-independent stimulation of PMNs from eight healthy humans towards two Staphylococcus saprophyticus strains (S 1 and S 35) was investigated. Strain S 1 was shown to have surface lectins with N-acetylgalactosamine specificity, whereas strain S 35 had N-acetyl-neuraminic acid specificity. Three different PMN-reaction patterns could be demonstrated: PMN stimulation was either sensitive to N-acetylgalactosamine-or N-acetylneuraminic acid-blocking, or resistant to both. These results point to the importance of lectins for staphylococcal-PMN interactions.

Acetylgalactosamine↗
PubMed1991

Plasma fibronectin and complement following infusion of colloidal solutions after spinal anaesthesia.

A randomized study of 30 patients undergoing uncomplicated surgery under spinal anesthesia was conducted to assess the influence of colloids on the kinetics of plasma fibronectin and complement. Both are opsonins of the reticuloendothelial system; moreover fibronectin is concerned with host resistance against septic complications following trauma and surgery. The patients were assigned to receive either Ringer's lactate (Group 1), gelatin (Group 2) or dextran 40 (Group 3). Blood samples were withdrawn before colloids or Ringer's infusion and during the 4 postoperative days. There was a reduction in plasma fibronectin throughout the study in groups 1 and 3, but an increase in group 2 by 24 h. The adhesion of plasma fibronectin to gelatin was maximal 1 h after infusion (44%) and remained significant up to day 2 in group 2. There was no relationship in groups 1 and 3. C3 and C4 components of complement exhibited a low value in the early post-operative period, due to hemodilution. This study shows an in vivo fibronectin-gelatin interaction, and suggests that gelatin infusion inhibits the increased shift of plasma fibronectin at the site of tissue injury after surgery.

Adult↗
PubMed1982

Fibronectin--mediator between cells and connective tissue.

Fibronectin, previously also termed LETS-protein, is a high-molecular-weight protein (mol. w. ca. 450,000) present in the form of thin fibrils in the pericellular space of fibroblasts and other adherent cells, as well as in distinct areas of the connective tissue. A soluble form, immunologically identical and chemically at least very similar to the cell-attached protein, is found in plasma in a concentration of about 300 micrograms/ml. It is also denominated cold-insoluble globulin. The protein has affinity both to cell surfaces and to various matrix substances such as fibrin and collagen and, therefore, is capable of mediating cell attachment to these substrates. In addition, it serves as an opsonin for the phagocytosis of gelatin-containing compounds and probably is essential for the removal of soluble fibrin from the circulating blood by the reticulo-endothelial system. Bacterial cell walls are also recognized by fibronectin. A conversion of soluble fibronectin to fibrils is achieved by heparin which also enhances the binding of soluble fibronectin to cells. Heparin or, as suggested, the related heparan sulfate present on the surface of various cells, appears to function as a cofactor in the formation of pericellular fibrils. The fibronectin fibrils precipitated with heparin, compared to soluble fibronectin, show a considerably improved affinity to native collagen, especially to type III. Hyaluronic acid has an antagonistic function which, at higher concentrations, prevents the fibronectin fibrils from interacting with collagen and cell surfaces. Masking of fibronectin fibrils was also achieved by sulfated proteoglycans of cartilage. Virus-transformed fibroblasts produce less fibronectin and are less capable of maintaining surface pericellular fibrils. A reasonable explanation is that they have an elevated secretion of hyaluronic acid. The transformed cells attach only weakly to a surface and exhibit a rounded shape in contrast to healthy ones. This phenotype can be corrected to a great extent with fibronectin. It is suggested that fibronectin also influences the formation of connective tissue by accumulating collagen precursors on the surface of fibroblasts and facilitating fibrillogenesis.

Cell Adhesion↗
PubMed1989

Host-parasite interaction in fungal infections.

The outcome of host-parasite interactions in fungal infections is determined by the balance between pathogenicity of the organism and the adequacy of the host defenses. A wide variety of host defense mechanisms are involved in protection against fungal infections. These include nonspecific mechanisms such as intact skin and mucus membranes, indigenous microbial flora, and the fungicidal activity of neutrophils and monocytes. Such mechanisms constitute the major host defense against opportunistic fungal infections caused by ubiquitous organisms of low virulence. The effective role of immunoglobulins and complement as opsonins varies with the fungal pathogen involved. Specific immune responses of both the humoral and cell-mediated type develop in response to infections by pathogenic fungi. Antibodies, in general, are not of major importance in protection against these infections. Specifically sensitized T lymphocytes produce lymphokines that activate macrophages. Activated macrophages are the major line of defense against systemic fungal pathogens. The type and degree of impairment in immune responses determines the susceptibility and severity of diseases. The type of immune response also determines the tissue reactions in these diseases and sometimes may be involved in the pathogenesis of the disease process. The role of natural killer cell activity, antibody-dependent cellular cytotoxicity, and biological response modifiers in various fungal infections has been described recently. The microbial factors of importance in fungal infections are adherence, invasion, presence of an antiphagocytic capsule, and ability to grow under altered physiological states of the host. The differences in the virulence of fungal strains is of minor importance in determining the outcome in general. The seriousness of the alteration of the host state rather than the pathogenic properties of the fungus determine the severity of the disease.

Animals↗
PubMed1993

Cefdinir-induced modification of the susceptibility of bacteria to the antibacterial activity of human serum and polymorphonuclear neutrophils.

The effect of serum on the bactericidal activity of cefdinir, and the ability of the antibiotic to modify the interaction of bacteria with human polymorphonuclear neutrophils were assessed. In the presence of antibiotic, serum-resistant Escherichia coli were sensitised to the bactericidal activity of normal human serum. Cefdinir enhanced opsonophagocytic killing of Escherichia coli and Staphylococcus aureus at suprainhibitory concentrations. Significant potentiation of killing occurred with the combination of inhibitory concentrations of cefdinir, neutrophils and sub-optimal levels of serum opsonins. Pre-exposure of Escherichia coli, but not Staphylococcus aureus, to cefdinir enhanced phagocytic uptake and killing of the antibiotic-damaged bacteria. These results indicate that cefdinir-mediated phenotypic modification of Escherichia coli renders the bacteria susceptible to serum antibacterial activity and phagocytic uptake and intracellular killing.

Bacteria↗