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PubMed1986

Effect of Tamm-Horsfall urinary glycoprotein on phagocytosis and killing of type I-fimbriated Escherichia coli.

Human polymorphonuclear leukocytes (PMN) ingest type I (mannose sensitive) fimbriated Escherichia coli even in the absence of antibody, complement, or other serum opsonins. Our studies suggest that the Tamm-Horsfall urinary glycoprotein (THP) interferes with serum-independent ingestion. Electron micrographs showed that dissolved THP adhered to type I fimbriae and formed a pseudocapsule around bacteria bearing type I fimbriae. Phase-variant bacteria grown on blood agar neither expressed fimbriae nor bound THP. Affinity column chromatography demonstrated mannose-sensitive binding between purified type I fimbriae and purified THP. The ability of human PMN to bind and ingest type I-fimbriated E. coli was diminished if the bacteria had been coated by exposure to THP at physiologic concentrations. At 1 h, PMN were associated with an average of 2.62 uncoated bacteria, but with only 0.18 coated bacteria (P less than 0.001). alpha-Methyl mannoside blocked the observed effect of THP on binding and phagocytosis in a dose-dependent fashion: increased mannoside led to increased blocking. PMN preincubated with THP were able to bind and phagocytose normally. There did not appear to be any significant clumping of bacteria in suspension to account for these effects. Bactericidal assays with leukocytes in suspension demonstrated protection of THP-coated bacteria. At 1 h, PMN killed 42% of noncoated E. coli (a decrease of 0.24 log), but the number of THP-coated bacteria increased by 75% (an increase of 0.24 log). These observations may partially explain the virulence of E. coli in the bladder and kidney, where serum activity is low and THP is abundant.

Adhesiveness↗
PubMed1986

Effect of macrophage activation on phagocyte-Plasmodium interaction.

We investigated the effect of both immune and normal sera on the binding of free Plasmodium berghei by resident and activated macrophages. Resident macrophages bound plasmodia to a greater extent than did activated macrophages, regardless of treatment. Resident macrophages bound free plasmodia, predominantly trophozoites, in the presence of normal serum by a mechanism inhibited by N-acetylglucosamine and N-acetylmannosamine. Macrophages activated through treatment with Propionibacterium acnes ("Corynebacterium parvum"), on the other hand, did not bind free plasmodia in the presence of normal serum through systems inhibited by N-acetylmannosamine or N-acetylglucosamine. The binding of free plasmodia by activated macrophages was greatest in the presence of immune serum and could be inhibited by immune complexes but not by N-acetylmannosamine or N-acetylglucosamine. These results suggest that a receptor for a carbohydrate component of a normal serum opsonin mediates initial adherence of plasmodial antigen onto resident macrophages, triggering both the immunological cascade and macrophage activation. After activation, the macrophages no longer have the carbohydrate-specific receptor but do have functional Fc receptors which mediate the adherence of immune-serum-opsonized plasmodia.

Animals↗
PubMed1986

Inhibition of macrophage phagocytosis by Bacteroides fragilis in vivo and in vitro.

A number of investigators have provided experimental evidence for synergistic effects in mixed infections with Escherichia coli and Bacteroides fragilis. In vitro studies have suggested that competition for serum opsonins and diminished subsequent phagocytosis by polymorphonuclear leukocytes might explain these effects. In the present study we evaluated the effect of B. fragilis on macrophage phagocytosis. It was shown that peritoneal macrophages from mice injected intravenously 6 to 12 h earlier with 10(8) CFU of encapsulated B. fragilis were markedly suppressed in their phagocytic ability. Injections of laboratory-passaged, less-encapsulated B. fragilis, other bacteria, or latex particles were either not suppressive of macrophage phagocytosis or less effective. When peritoneal macrophages were treated in vitro for 24 h with the same challenge organisms prior to assessing their phagocytic capacity, encapsulated B. fragilis also proved significantly more suppressive than challenges with other organisms or latex particles. We conclude that suppression of macrophage phagocytosis by B. fragilis seems to be an important mechanism contributing to synergistic effects described for mixed aerobic and anaerobic infections.

Animals↗
PubMed1986

Nonopsonic phagocytosis of nonmucoid Pseudomonas aeruginosa by human neutrophils and monocyte-derived macrophages is correlated with bacterial piliation and hydrophobicity.

We have shown previously that some strains of Pseudomonas aeruginosa from patients with cystic fibrosis are phagocytized by human polymorphonuclear leukocytes in the absence of serum opsonins. The purpose of this study was to identify the bacterial features which render certain strains susceptible to nonopsonic phagocytosis. Three strains were phagocytized by human neutrophils and monocyte-derived macrophages, and two were not, as determined by luminol-enhanced chemiluminescence, visual inspection of stained smears, and bactericidal assay. Strains that were phagocytized formed pellicles when grown in static broth, but the phagocytosis-resistant strains did not. The phagocytosis-susceptible strains were more heavily piliated and more hydrophobic than the resistant strains. Bacteria exposed to heat (60 degrees C) or UV irradiation were depiliated, as assessed by electron microscopy, and rendered resistant to phagocytosis. When P. aeruginosa was grown on agar, it was piliated, hydrophobic, and susceptible to nonopsonic phagocytosis, but when grown to stationary phase in shaken broth, it was nonpiliated, less hydrophobic, and resistant to phagocytosis. It appears that nonopsonic phagocytosis of certain P. aeruginosa strains by human polymorphonuclear leukocytes and macrophages is facilitated by hydrophobic interactions which may be determined in part by pili.

Adult↗
PubMed1987

Colonial dissociation and susceptibility to phagocytosis of Pseudomonas aeruginosa grown in a chamber implant model in mice.

Pseudomonas aeruginosa strains were grown in 1-cm plastic chambers sealed at both ends with porous Millipore filters and implanted in the peritonea of mice. Mucoid and nonmucoid strains of P. aeruginosa isolated from a patient with cystic fibrosis largely retained their phenotypes when grown for up to 1 year in this in vivo system, although colonial dissociation occurred, as observed in chronic lung infections of patients with cystic fibrosis. In the absence of added opsonins, P. aeruginosa M2 cells taken directly from the in vivo system were significantly more susceptible to phagocytosis than were the same P. aeruginosa cells after being washed in buffer. Phagocytosis of in vivo-grown P. aeruginosa cells could be further enhanced by using a porin protein F-specific monoclonal antibody.

Antibodies, Bacterial↗
PubMed1987

Factors influencing the phagocytosis of Clostridium difficile by human polymorphonuclear leukocytes.

Phagocytosis of Clostridium difficile by human polymorphonuclear leukocytes (PMNs) and the possible role of the clostridial toxins in this process were investigated. Phagocytosis of C. difficile was independent of aerobiosis and clearly depended on opsonization. Either complement or antibodies to C. difficile could serve as opsonins. Toxigenic strains of C. difficile were more resistant to phagocytosis than were nontoxigenic strains. Pretreatment of PMNs with as much as 10,000 units of toxins from culture filtrates of C. difficile for 2 h had no effect on either the phagocytic activity of PMNs or their viability as determined by trypan blue exclusion. In contrast, treatment of human embryonic intestinal cells with the same amount of toxin under identical conditions resulted in cell death.

Aerobiosis↗
PubMed1988

Alginase treatment of mucoid Pseudomonas aeruginosa enhances phagocytosis by human monocyte-derived macrophages.

Mucoid Pseudomonas aeruginosa colonizes and infects the respiratory tract of most older patients with cystic fibrosis. These bacteria resist both opsonin-dependent and -independent phagocytosis by human polymorphonuclear leukocytes and monocyte-derived macrophages. Resistance to phagocytosis is thought to be mediated in part by the mucoid exopolysaccharide associated with the bacterial surface. The purpose of this study was to determine whether degradation of the mucoid exopolysaccharide by alginase enhances bacterial susceptibility to nonopsonic phagocytosis by macrophages. Eight phagocytosis-resistant mucoid P. aeruginosa isolates from patients with cystic fibrosis were studied. The bacteria were treated with a preparation of alginase from Bacillus circulans, and phagocytosis by macrophages was measured by a visual inspection assay. Alginase degradation of mucoid exopolysaccharide was measured by the periodate-thiobarbituric acid assay and by indirect immunofluorescence with a mouse monoclonal antibody to the mucoid exopolysaccharide. Alginase degraded the mucoid exopolysaccharide of all eight mucoid strains tested. Phagocytosis was enhanced in five of the eight strains. Alginase-enhanced phagocytosis was magnesium dependent and heat labile. Alginase may be a useful tool for studying the biological properties of P. aeruginosa mucoid exopolysaccharide.

Antibodies, Monoclonal↗
PubMed1989

Lectinlike interactions of Fusobacterium nucleatum with human neutrophils.

Fusobacterium nucleatum expresses lectinlike adherence factors which mediate binding to a variety of human tissue cells. Adherence is selectively inhibited by galactose, lactose, and N-acetyl-D-galactosamine. In this study, adherence of F. nucleatum to human peripheral blood polymorphonuclear neutrophils (PMNs) was investigated. The results indicated that the fusobacteria adhered to live and metabolically inactivated or fixed PMNs. Adherence of F. nucleatum resulted in activation of PMNs as determined by PMN aggregation, membrane depolarization, increased intracellular free Ca2+, superoxide anion production, and lysozyme release. Transmission electron micrographs showed that F. nucleatum was phagocytized by the PMNs. Microbicidal assays indicated that greater than 98% of F. nucleatum organisms were killed by PMNs within 60 min. Adherence to and activation of PMNs by F. nucleatum were inhibited by N-acetyl-D-galactosamine or lactose greater than galactose, whereas equal concentrations of glucose, N-acetyl-D-glucosamine, mannose, and fucose had little or no effect on F. nucleatum-PMN interactions. Pretreatment of the fusobacteria with heat (80 degrees C, 20 min) or proteases inhibited adherence to and activation of PMNs, but superoxide production was also stimulated by heated bacteria. The results indicate that interaction of F. nucleatum with PMNs is lectinlike and is probably mediated by fusobacterial proteins which bind to other human tissue cells. Adherence of F. nucleatum to PMNs in the absence of serum opsonins, such as antibodies and complement, may play an important role in PMN recognition and killing of F. nucleatum in the gingival sulcus and in the subsequent release of PMN factors associated with tissue destruction.

Bacterial Adhesion↗
PubMed1990

Tumor necrosis factor enhances neutrophil-mediated killing of Plasmodium falciparum.

We developed a radiometric assay by which the antiplasmodial effects of phagocytic cells can be quantitated. This assay was used to examine the effects of recombinant human tumor necrosis factor alpha (TNF-alpha) on the killing of Plasmodium falciparum by human neutrophils. Data presented demonstrated that neutrophils engulf and destroy P. falciparum, but substantial killing of parasites required the presence of either heat-labile or heat-stable opsonins. While recombinant TNF-alpha at concentrations of 5 to 50,000 U/ml showed no direct effects on the parasite, this cytokine augmented the antimalarial activity of neutrophils at doses of 20 to 250 U/10(6) neutrophils. The results suggest that TNF-alpha is an important component of the immune phagocytic effector mechanisms which are involved in destruction of the malarial parasite.

Animals↗
PubMed1991

Immunogenicity of Actinobacillus pleuropneumoniae outer membrane proteins and enhancement of phagocytosis by antibodies to the proteins.

To determine the opsonic effect of antibodies to Actinobacillus (Haemophilus) pleuropneumoniae outer membrane proteins on phagocytosis by porcine polymorphonuclear leukocytes (PMN), we separated the integral outer membrane proteins (IOMPs) by Triton X-114 extraction. Four major IOMPs with molecular masses of 76, 50, 39, and 29 kDa were detected by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. These IOMPs were found to be essentially free of endotoxin in the Limulus amebocyte lysate assay. The 76-kDa protein exhibited a more intensely stained electrophoresis band when isolated from iron-restricted cultures, and a new band at 105 kDa was present in the whole-membrane fraction but not in the integral fraction, indicating that the 105-kDa iron-repressible protein is a peripheral membrane protein. The 76-, 50-, and 39-kDa proteins were shown to be surface exposed, since antibodies to these IOMPs could be absorbed out of convalescent-phase sera by whole cells. Percentages of phagocytosis by porcine PMN of A. pleuropneumoniae opsonized with convalescent-phase sera, convalescent-phase sera absorbed with IOMPs, or convalescent-phase sera absorbed with whole cells were 46.75, 21.81, and 7.96%, respectively. These results demonstrate that antibodies to IOMPs of A. pleuropneumoniae serve as important opsonins in phagocytosis by porcine PMN.

Actinobacillus↗
PubMed1992

Arg-Gly-Asp (RGD) peptides alter hepatic killing of Candida albicans in the isolated perfused mouse liver model.

The isolated perfused mouse liver model was used to study the effect of Arg-Gly-Asp (RGD)-containing peptides on hepatic trapping and killing of Candida albicans. After extensive washing, 10(6) C. albicans CFU were infused into mouse livers. At the time of recovery, 63% +/- 2% (mean +/- standard error of the mean) of the infused C. albicans CFU were recovered from the liver and 14% +/- 1% were recovered from the effluent for a total recovery of 77% +/- 2%. This indicates that 86% +/- 9% of the original inoculum was trapped by the liver and that 23% +/- 2% was killed within the liver. Prior to their infusion into livers, 10(7) CFU of C. albicans were incubated at 37 degrees C for 30 min in the presence of various RGD peptides (0.1 mg/ml). Repeatedly, more than 90% of the infused RGD-treated C. albicans was trapped by the perfused liver. In comparison with the 23% killing rate observed in control livers, perfused livers killed approximately 40 to 50% of the infused C. albicans treated either with fibronectin, PepTite 2000, RGD, or RGDS. Hepatic killing of C. albicans treated with PepTite 2000 or fibronectin was dose dependent. Treatment of C. albicans with GRGDTP, GRGDSP, GRADSP, or GRGESP did not alter the ability of the perfused liver to kill C. albicans, suggesting that a degree of specificity for RGD peptides is associated with an increased ability of liver to kill RGD-treated C. albicans. Together, the data suggest that RGD peptides bind to a receptor on the surface of C. albicans, thereby increasing hepatic, and presumably Kupffer cell, killing of C. albicans. Natural or synthetic RGD peptides may serve as opsonins promoting C. albicans killing by Kupffer cells.

Amino Acid Sequence↗
PubMed1992

S-layer-mediated association of Aeromonas salmonicida with murine macrophages.

The interaction of Aeromonas salmonicida with the murine macrophage (M phi) cell line P388D1 was used as a convenient model to study the involvement of the bacterial crystalline surface array (or A-layer) in the association with M phi s. A-layer-positive (A+) cells readily associated with M phi s in phosphate-buffered saline, whereas A- mutants were unable to do so, even when the bacterium-M phi interaction was forced by centrifugation. M phi s selectively interacted with A+ cells when challenged with mixtures of A+ and excess A- cells. Electron microscopy indicated that in phosphate-buffered saline only A+ bacteria were readily internalized, although by a nonconventional mechanism, suggesting that efficient phagocytosis in the absence of opsonins was A-layer mediated. Latex beads coated with a partially assembled A-layer were more efficiently taken up than uncoated or A-protein-coated beads, indicating that an organized A-layer was essential for M phi uptake. The reduced ability of M phi s plated on a substratum coated with the A-layer to bind A+ bacteria also suggested that association was both A-layer and receptor mediated. In the presence of tissue culture medium, competent M phi s interacted efficiently with A- bacteria and internalized them through conventional phagocytosis. A+ cells were markedly cytotoxic to M phi s, whereas the A-protein or A-layer was not. A- cells were cytotoxic to a lesser extent, suggesting that cytotoxicity was targeted.

Aeromonas↗
PubMed1992

Preparation, characterization, and immunogenicity of conjugate vaccines directed against Actinobacillus pleuropneumoniae virulence determinants.

Conjugate vaccines were prepared in an attempt to protect pigs against swine pleuropneumonia induced by Actinobacillus pleuropneumoniae (SPAP). Two subunit conjugates were prepared by coupling the A. pleuropneumoniae 4074 serotype 1 capsular polysaccharide (CP) to the hemolysin protein (HP) and the lipopolysaccharide (LPS) to the HP. Adipic acid dihydrazide was used as a spacer to facilitate the conjugation in a carbodiimide-mediated reaction. The CP and the LPS were found to be covalently coupled to the HP in the conjugates as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and detergent gel chromatography analyses. Following a booster vaccination, pigs exhibited significantly high (P less than 0.05) immunoglobulin G antibodies against CP, LPS, and HP. The anti-CP and anti-LPS immunoglobulin G antibodies were found to function as opsonins in the phagocytosis of A. pleuropneumoniae by polymorphonuclear leukocytes, whereas antibodies to the HP neutralized the cytotoxic effect of the HP on polymorphonuclear leukocytes. No killing of A. pleuropneumoniae was observed when the effects of the antibodies were tested in the presence of complement. Thus, polysaccharide-protein A. pleuropneumoniae conjugates elicit significant antibody responses against each component of each conjugate, which could be instrumental in protecting swine against SPAP.

Actinobacillus pleuropneumoniae↗
PubMed1993

Shigella flexneri transformants expressing type 1 (mannose-specific) fimbriae bind to, activate, and are killed by phagocytic cells.

Shigella flexneri M90T (invasive) and BS176 (noninvasive) are typical nonfimbriated organisms that do not bind to or activate phagocytic cells. We demonstrate that S. flexneri M90Tp and BS176p, obtained by transformation of the strains named above with the cluster of genes encoding type 1 (mannose-specific) fimbriae of Escherichia coli, express the functional fimbriae, as shown by electron microscopy, by binding of antifimbria antibodies and by yeast cell aggregation. The transformants, but not the parental strains, bound to human granulocytes and mouse peritoneal macrophages. This binding was inhibited by methyl alpha-D-mannoside but not by methyl alpha-D-galactoside. The bound bacteria induced oxidative burst activation and degranulation of the granulocytes in vitro. With mouse peritoneal macrophages, the binding of the fimbriated bacteria induced degranulation in vitro. Injection of the bacteria into mouse peritoneum also induced degranulation of the macrophages in vivo; no such effect was observed with the nonfimbriated strains. The bound fimbriated transformants were effectively killed by the human granulocytes in vitro in the absence of opsonins or after opsonization with human anti-S. flexneri antiserum. The nonfimbriated strains were killed only after opsonization. These results provide further evidence for the role of type 1 fimbriae in lectin-mediated nonopsonic phagocytosis.

Animals↗
PubMed1993

Mechanisms of nonopsonic phagocytosis of Pseudomonas aeruginosa.

The interaction of the macrophage cell line P388D1 with Pseudomonas aeruginosa in the absence of stimulators or opsonins led to substantial association of bacteria, as judged by visual counting and FACScan assays. This association was observable within 5 min of addition of bacteria, could not be disturbed by exhaustive washing, and occurred with pilus- or flagellum-deficient mutants but not with rpoN mutants, which have been proposed to lack a secondary adhesin. In contrast, specific antibody was capable of causing similar enhancement of bacterial uptake regardless of the rpoN phenotype. Fibronectin stimulated uptake of bacteria with the pilus as an adhesin, and stimulation was observable within 5 min. Both fibronectin-enhanced and antibody-opsonized uptake were susceptible to inhibition by pertussis toxin but not by cholera toxin. The influence of fibronectin on P388D1 cells was distinguishable from that of lipopolysaccharide, which caused substantial morphological changes in cells. Although lipopolysaccharide stimulated bacterial uptake, it actually suppressed fibronectin-mediated enhancement of uptake at high concentrations.

Adhesins, Bacterial↗
PubMed1994

Polysaccharide capsule-mediated resistance to opsonophagocytosis in Klebsiella pneumoniae.

The polysaccharide capsule of Klebsiella pneumoniae is an important virulence factor that confers resistance to phagocytosis. The treatment of encapsulated bacteria with salicylate to inhibit capsule expression was found to enhance the phagocytosis of encapsulated bacteria by human neutrophils only in the presence of cell surface-specific antibodies. Both type-specific rabbit antisera and anticapsular human hyperimmune globulin were employed as opsonins. Salicylate significantly enhanced phagocytosis with homologous, but not heterologous, whole-cell antisera. Antisera, diluted 1:40, no longer opsonized fully encapsulated bacteria but promoted the uptake of multiple salicylate-treated bacteria in > 90% of neutrophils. Salicylate (0.25 to 1.0 mM) also enhanced opsonization with globulin against homologous bacteria. Higher salicylate levels (1 to 2.5 mM) enhanced the opsonization of heterologous serotypes with human globulin. The nature of antibody attachment to encapsulated bacteria was determined by immunofluorescence. Even after the addition of purified capsular polysaccharide to prevent phagocytosis, K-specific antibodies attached in large amounts to bacteria. K-specific antibodies reacted with antigens throughout the capsule and showed a predilection for a denser inner layer of the capsule, indicating that many of the K-specific antibodies may be masked underneath the capsule surface. K-specific antibodies can also be rendered nonfunctional by soluble, cell-free capsular antigen. In culture, large quantities of soluble capsular polysaccharide extrude from bacteria after overnight growth. The reduction in capsule expression caused by salicylate largely affected the soluble, cell-free fraction. Purified capsular polysaccharide was shown to retard the opsonophagocytosis of salicylate-treated bacteria in a concentration-dependent manner. However, extensive washing of encapsulated bacteria to remove loosely attached capsular material did not significantly enhance opsonophagocytosis. In conclusion, cell-free capsule and cell-associated capsule are antiphagocytic; both act to neutralize K-specific antibodies by binding or concealment. Salicylate-mediated inhibition of capsule expression, particularly of the cell-free fraction, improved K-specific opsonization dramatically.

Animals↗
PubMed1994

Functional activity of antibodies to the group B polysaccharide of group B streptococci elicited by a polysaccharide-protein conjugate vaccine.

Group B streptococci (GBS) are a major cause of sepsis and meningitis in infants. While antibodies directed to the type-specific GBS capsule have been shown to be protective, it is less clear whether antibodies to the group B polysaccharide, a noncapsular, cell wall-associated antigen, may play a role in immunity. To investigate the functional activity of group B polysaccharide-specific antibodies, we tested sera from rabbits vaccinated with group B polysaccharide coupled to tetanus toxoid (B-TT). Anti-B-TT was weakly opsonic in vitro for a highly encapsulated type III strain, while antiserum elicited by vaccination with type III capsular polysaccharide linked to tetanus toxoid (III-TT) was a very effective opsonin. In contrast to anti-III-TT, anti-B-TT given before or after bacterial challenge was only marginally effective in protecting newborn mice against lethal infection with type III GBS. The number of C3 molecules bound to type III GBS was augmented by anti-III-TT but not by high antibody concentrations of anti-B-TT. These results suggest that the difference in opsonic activity between anti-B-TT and anti-III-TT may be due to a difference in their ability to deposit C3. In addition, the maximum number of antibody molecules bound to the bacterial surface was greater for anti-III-TT than for anti-B-TT. That anti-B-TT binds to fewer sites than anti-III-TT may explain the differences in complement activation and in opsonic and protective efficacy of antibodies to group B polysaccharide compared with antibodies to the type-specific capsular polysaccharide.

Animals↗
PubMed1994

Streptococcus uberis resists the bactericidal action of bovine neutrophils despite the presence of bound immunoglobulin.

Streptococcus uberis 0140J was more resistant to the bactericidal action of bovine neutrophils after growth in chemically defined medium (CDM) supplemented with casein hydrolysate than when grown in CDM alone. Neither adult bovine serum obtained prior to vaccination nor hyperimmune serum raised against this bacterium was capable of acting as an effective opsonin towards S. uberis grown in the presence of casein hydrolysate. There was no detectable difference in the ability of bacteria grown in either CDM or CDM supplemented with casein hydrolysate to bind immunoglobulin G1 (IgG1), IgG2, or IgM from either hyperimmune serum or preparations of immunoglobulin from the same serum. Bacteria of both the phagocytosis-resistant and phagocytosis-sensitive phenotypes presented the same amount of IgG2 Fc terminus on their surfaces. It is concluded that the inducible resistance of S. uberis to bactericidal action of bovine neutrophils is not mediated by inhibition of antibody binding.

Animals↗