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PubMed1990

Comparison of cefodizime with various cephalosporins for their indirect effect on the human neutrophil oxidative burst in vitro.

Cefodizime, a 2-amino-thiazolyl cephalosporin, is reported to display in-vitro, ex-vivo and in-vivo immunomodulatory properties; in particular, it enhances the survival of mice infected with cefodizime-resistant pathogens. We have used an in-vitro model to assess the indirect effect of this drug (compared with other cephalosporins) on the neutrophil (PMN) oxidative response. Pseudomonas aeruginosa was employed as the bacterial target for cefodizime and cefotaxime (MICs greater than 128 mg/l), cefsulodin (MIC 16 mg/l) and ceftazidime (MIC 32 mg/l). After overnight growth in the presence of subinhibitory concentrations of each drug (10 mg/l), the altered filamentous P. aeruginosa induced a stronger oxidative response of PMN than untreated control bacteria. For all cephalosporins this was related to alterations of bacterial structure leading to increased deposits of antibodies and/or complement. Furthermore, increased non-opsonin dependent stimulation of the PMN oxidative burst was obtained; the strongest response was observed with cefodizime-treated P. aeruginosa in the case of low responder PMN, which displayed a deficient response after stimulation by control bacteria. The possibility that cefodizime could enhance this PMN function in opsonin-deficient patients requires further investigation.

Cefotaxime↗
PubMed1980

Comparative studies on alveolar macrophages and polymorphonuclear leukocytes. I. H2O2 and O2- generation by rabbit alveolar macrophages.

The oxidative metabolism of rabbit alveolar macrophages (A-MO) was compared with that of rabbit polymorphonuclear leukocytes (PMN) with respect to H2O2 generation by intact cells or subcellular fractions. Rabbit PMN exhibited an increase in the oxygen uptake and a marked release of H2O2 upon addition of heat-killed E. coli in the presence and absence of opsonin. However, rabbit A-MO exhibited an increase in the oxygen uptake upon addition of E. coli only in the presence of anti-E. coli serum as an opsonin, whereas a very small amount of H2O2 release was observed during ingestion of the opsonized E. coli. The generation of O2- and H2O2 by a granule-rich fraction isolated from phagocytosing PMN was larger than that by a similar fraction isolated from resting PMN. However, there was no significant difference in O2- and H2O2 generation by the granule fractions between phagocytosing and resting A-MO in the presence of either NADH or NADPH. In contrast to the granule fraction of rabbit PMN, the O2- and H2O2 generating activities in the A-MO granule fraction were higher in the presence of NADH than in the presence of NADPH. The rates of NADH and NADPH oxidation by both A-MO and PMN granule fractions were measured with and without addition of Mn2+ to the assay medium. The effect of Mn2+ on the NAD(P)H oxidase was found to differ between rabbit A-MO and PMN.

Animals↗
PubMed2003

Immunity to Streptococcus pneumoniae: Factors affecting production and efficacy.

Streptococcus pneumoniae is a complex human pathogen and a major cause of morbidity and mortality. The genetic background of pneumococci and the chemical structure of their capsules is largely unraveled as well as the basic role of anticapsular antibodies and other opsonins interacting to enhance phagocytosis. Many experimental studies are improving our knowledge on the complex molecular mechanisms underlying those events. Pneumococcal optimal clearance requires the cooperation of a plethora of reactions from both innate and adaptive immunity. The last advances in the complexity of the immune response and protection are reviewed: phagocyte-pneumococcus interactions mediated by opsonins; the role of complement, reactive C protein and natural antibodies; details of novel immune evasion mechanisms; the complex role of the inflammatory mediators in the susceptibility to pneumococcal infections; why capsular polysaccharides do not yield an anamnestic response after primary immunization; the central question of whether T cells regulate in-vivo anti-polysaccharide immunoglobulin responses to intact pathogens. All of these are topics where new data and some answers are offered. The state of the art on the research of pneumococcal protein vaccines as an alternative to plain polysaccharide or conjugated vaccine and the establishment of immunologic correlates of protection to facilitate efficacy trial assessment are also reviewed.

Animals↗
PubMed1987

Interaction of Campylobacter pyloridis with human immune defence mechanisms.

The in-vitro susceptibility to host immune defence mechanisms of Campylobacter pyloridis was investigated. C. pyloridis was sensitive to antibody-dependent complement-mediated bactericidal activity of serum. The bacteria were phagocytosed and efficiently killed by polymorphonuclear neutrophils in the presence of serum opsonins. Serum opsonin depletion studies indicated that an intact classical complement pathway was required for optimal phagocytic killing.

Blood Bactericidal Activity↗
PubMed1993

Exposure to complement-bearing immune complexes enhances the in vitro sequestration of erythrocytes from young but not elderly donors.

Complement and immunoglobulin have each been claimed to be the major opsonins responsible for sequestration of the effete erythrocyte. Binding of immune complexes to the erythrocyte via CR1 (CD35) provides a model for studying the effects of increments in membrane-bound complement and immunoglobulin on the sequestration of the erythrocyte ('innocent bystander' sequestration). It is possible that C3b-bearing immune complexes (IC-C3b) bound to erythrocyte CR1 contribute to the levels of immunoglobulin and complement fragments detectable on the human erythrocyte. We have, therefore, compared the capacity of erythrocytes from young and elderly donors to bind IC-C3b and the effect of this binding on in vitro sequestration. Erythrocytes from young donors exposed to IC-C3b bind these complexes, as attested by an increment in membrane-bound C3, and undergo 'innocent bystander' sequestration. However, when density-separated erythrocytes are so exposed, it is only the low density (young) erythrocytes from young donors which are susceptible to 'innocent bystander' sequestration. High density (old) erythrocytes from young donors and all erythrocytes from elderly donors show initially high in vitro sequestration and are resistant to the 'innocent bystander' effect. (Those erythrocytes which show initially high in vitro sequestration are referred to collectively as 'in situ aged' erythrocytes.) There is a great similarity between the mechanisms of sequestration of 'in situ aged' and 'innocent bystander' erythrocytes in that they are both inhibited by the integrin binding peptide arginine-glycine-aspartic acid (RGD) and the beta-galactosyl sugar N-acetyl-galactosamine, and unaffected by the Fc-gamma binding protein, Protein-G. Complement is the major opsonin in 'innocent bystander' sequestration since this sequestration occurs whether the isotype of the antibody in the immune complex is IgM or IgG, and Protein-G, which inhibits IgG-dependent erythrophagocytosis, has no effect on 'innocent bystander' sequestration. The present studies demonstrate that in vitro sequestration of 'in situ aged' erythrocytes is similar to complement-dependent 'innocent bystander' sequestration, thus supporting the contention that complement recognition is cardinal in sequestration of 'in situ aged' erythrocytes.

Adolescent↗
PubMed1983

Complement (C3)-receptor-mediated phagocytosis of agarose beads by mouse macrophages. II. Extracellular activation of macrophage-derived complement on agarose via the alternative pathway.

Phagocytosis of agarose beads by macrophages cultured under serum-free conditions was studied. 48 h was needed before a plateau in the uptake was reached. The ingested agarose beads were coated extracellularly with macrophage-derived protein before attachment and ingestion of the beads. Intracellularly, the agarose-linked protein was removed from the agarose. If the ingested agarose beads were extracted from the macrophages within 24 h after the plateau in the uptake was reached, a fraction of the beads could attach to new macrophages, demonstrating modification of the agarose beads by opsonin(s). Because of binding of anti-human C3c antibodies to beads extracted from the macrophages after 24 h of phagocytosis and the trypsin sensitivity of the protein on the agarose, we conclude that the main opsonin on the agarose beads is C3bi. Requirements for the stimulatory effect of agarose on macrophages are summarized.

Animals↗
PubMed1998

Attachment of group B streptococci to macrophages is mediated by a 21-kDa protein.

Group B Streptococcus (GBS) is able to bind to human macrophages in vitro in the absence of exogenous opsonins. The exact mechanisms that mediate this attachment are unclear. This study was undertaken to determine what protein adhesins are present on the surface of GBS that mediate attachment to macrophages. We have identified a 21-kDa protein from the envelope of GBS type III that directly binds to macrophages as determined by Western blot analysis. Antiserum against this protein was able to inhibit binding of GBS to macrophages by greater than 80% as measured by flow cytometry. Antiserum against the 21-kDa protein cross-reacted with 21-kDa proteins from GBS type Ib, type II, type III (COH31 and MR732) and type IV, as well as Staphyloccus epidermidis, but not GBS type Ia, Listeria monocytogenes or Enterococcus faecalis. This protein may be important in mediating the attachment of GBS to macrophages in an opsonin-poor environment.

Antibodies, Bacterial↗
PubMed1991

Difference in the protection against infection with different challenge strains of Salmonella enteritidis by killed vaccine.

Differences in protection against the challenge of different strains of formalin-killed cells obtained from Salmonella enteritidis were investigated. When strains 2547, 116M, 116-54, SR-98G, and 3775 were used as the challenge strain, protective effects were apparent in groups of mice immunized with formalin-killed cells from S. enteritidis strains (protective strains). Conversely, no protective effects were observed with the challenge of strains 2822, 3975, and IID-604 (nonprotective strains). Electrophoretic banding patterns of lipopolysaccharides in SDS-PAGE were similar between the LPS obtained from the various strains used in this study. Additionally, no differences in sensitivity to macrophage intracellular killing were observed between the protective and nonprotective strains. Phagocytic experiments by macrophages in vitro indicated that immune serum used as the opsonin promotes phagocytosis of various strains by macrophages as compared to using normal serum as the opsonin, but the rate of phagocytosis enhanced by immune serum is higher in protective strains than nonprotective strains. In studies of passive transfer of immune serum, it was found that mice passively immunized with immune serum could only protect against infection by challenging with protective strains with the exception of strain SR-98G. These results suggest that the protective effect observed with the challenge of protective strains may be due to macrophage phagocytosis enhanced by opsonization with immune serum.

Animals↗
PubMed1995

Subinhibitory concentrations of cefpodoxime alter membrane protein expression of Actinobacillus actinomycetemcomitans and enhance its susceptibility to killing by neutrophils.

The aim of the present study was to determine the effect of the antibiotic cefpodoxime on the gram-negative periodontopathic microorganism Actinobacillus actinomycetemcomitans and its interaction with elements of the host immune system. Growth of A. actinomycetemcomitans in subinhibitory concentrations of cefpodoxime induced morphological changes in the bacteria, causing the organisms to grow as filaments rather than coccobacilli. Growth in cefpodoxime did not render these bacteria susceptible to killing by serum, nor did it abrogate the requirement for serum opsonins to support the bactericidal activity of neutrophils. Cefpodoxime enhanced the susceptibility of A. actinomycetemcomitans to the bactericidal activity of neutrophils. In the presence of suitable opsonins, neutrophils were able to kill four times as many cefpodoxime-induced A. actinomycetemcomitans filaments as untreated A. actinomycetemcomitans CFU. This effect was due to antibiotic actions on the bacterium and not on the neutrophil. At inhibitory concentrations, the bactericidal activities of cefpodoxime and neutrophils were additive, and cefpodoxime did not interfere with the normal functioning of the neutrophils. Concomitant with these morphological and functional changes, the expression of two outer membrane proteins (66 and 29 kDa) and one inner membrane protein (57 kDa) was decreased in A. actinomycetemcomitans grown in cefpodoxime. The concentration range over which cefpodoxime is effective against A. actinomycetemcomitans in vivo may be extended by the ability of subinhibitory concentrations to enhance the susceptibility of this organism to host immune defenses.

Adult↗
PubMed1979

Chemotaxigenesis and activation of the alternative complement pathway by encapsulated and non-encapsulated Cryptococcus neoformans.

In the presence of serum, whole cells of encapsulated and non-encapsulated Cryptococcus neoformans generated a chemotactic response by neutrophils. Heat inactivation of serum ablated all chemotactic activity. Cryptococcal polysaccharide was not chemotaxigenic. Assays for alternative complement pathway activation such as depletion of alternative complement pathway factor B or electrophoretic conversion of factor B closely paralleled chemotaxis assays. Cells of encapsulated and non-encapsulated C. neoformans activated the alternative complement pathway, whereas cryptococcal polysaccharide was inactive. Failure of the capsular material to activate the alternative pathway was not due to serotype specificity because polysaccharide of several serotypes failed to achieve activation. The results suggest that chemotaxigenesis and alternative complement pathway activation are functions of the yeast cell wall. The results support our proposal that the cryptococcal capsul does not prevent potential opsonins from reaching binding and activation sites at the yeast cell wall or the release of biologically active soluble cleavage products into the surrounding medium; however, cell wall-bound cleavage products remain bound to the cell wall beneath the capsule. Therefore, they are unable to participate as opsonins in phagocytosis.

Animals↗
PubMed1987

Functional capacity of marginated and bone marrow reserve granulocytes.

Marginated and bone marrow reserve granulocytes were obtained from young healthy volunteers after subcutaneous administration of aqueous epinephrine (0.4 ml/m2) or intravenous administration of hydrocortisone sodium succinate (250 mg), respectively. These leukocytes were compared with circulating granulocytes for the ability to adhere to surfaces, migrate in a random fashion, respond to chemoattractants, interact with autologous serum opsonins, and phagocytize and kill five common bacterial pathogens. As contrasted with circulating neutrophils, marginated cells had enhanced phagocytic and killing capacity for some pathogens, whereas adherence, random migration, chemotaxis, and chemiluminescence for the two cell populations were equivalent. Bone marrow reserve cells demonstrated increased activity for three functional mechanisms; chemotaxis for these cells averaged 21% higher than that for circulating cells, and phagocytosis was 32% higher, with 6 to 17% greater killing of the five bacterial species studied. All of these differences were statistically significant (P less than 0.05). Random migration and interaction with serum opsonins were unchanged in bone marrow granulocytes. These enhanced functional properties of neutrophils which are outside of the circulating pool may represent important host defense mechanisms during episodes of bacterial infection.

Bacteria↗
PubMed1989

Energy is required for maximal adherence of Neisseria gonorrhoeae to phagocytic and nonphagocytic cells.

The possibility that gonococcal energy might play a role in the interaction of Neisseria gonorrhoeae with both phagocytic and nonphagocytic cells was examined. Respiratory chain inhibitors including KCN and amobarbital resulted in reduction in gonococcal association with human neutrophils. Similar results were seen with HeLa cells and the human promyelocytic (HL-60) cell line. Identical conditions did not affect the opsonin-dependent association of Staphylococcus aureus with the same cell types. New protein synthesis by gonococci did not account for the observed reduction in association. These results suggest that energy is needed for maximal opsonin-independent association of gonococci with mammalian cells.

Aerobiosis↗
PubMed1992

Interaction of the fish pathogen Aeromonas salmonicida with rainbow trout macrophages.

A procedure was developed to culture rainbow trout macrophages (M phi) on supported glass coverslips. Using this method and a variety of well-characterized Aeromonas salmonicida strains with normal or altered cell surfaces, we investigated the role of this unusual bacterial surface in the bacterium-M phi interaction. An intact crystalline protein array, the A-layer, mediated adherence of A. salmonicida cells to M phi even in the absence of opsonins. In contrast, unopsonized cells of an A-layer-negative (A-) mutant with a smooth lipopolysaccharide (LPS) layer were unable to interact with M phi. However, this ability was recovered when the A-layer was reconstituted onto the smooth LPS surface of these A- LPS+ cells. Two A. salmonicida mutants possessing the A-layer in different disorganized states had a reduced ability to interact with M phi. A+ cells grown under calcium limitation produced A-layers locked into an alternative conformation which mediated the highest levels of M phi association in the absence of opsonins or any other surface coating. Coating A+ cells with hemin greatly increased their levels of M phi association, and bacterial cells grown on trout blood agar plates also had a dramatic increase in their ability to interact with M phi. Only A+ A. salmonicida cells were highly cytotoxic to trout M phi, especially after being coated with hemin, presumably due to a more focused targeting of the bacterial cell onto the M phi surface and/or into the intracellular regions of the M phi.

Aeromonas↗
PubMed1998

Role of CR4 in Mycobacterium tuberculosis-human macrophages binding and signal transduction in the absence of serum.

The beta2 integrin CR4 is involved in Mycobacterium tuberculosis phagocytosis by human mononuclear phagocytes through the opsonin C3bi. In this study, we demonstrate that M. tuberculosis can bind directly to monocyte-derived macrophages via CR4 in the absence of any opsonins. CR4-transfected CHO cells gave similar results, suggesting recognition by CR4 of bacterial structure. Furthermore, binding of M. tuberculosis transduced a potent signal, resulting in tyrosine phosphorylation of macrophage proteins, which was in part mediated by CR4.

Animals↗
PubMed2003

Phagocytic activity and monocyte chemotactic protein expression by pulmonary macrophages in persistent pulmonary cryptococcosis.

The mechanisms by which Cryptococcus neoformans persists in an immunocompetent host are not well understood. Using a rat model of persistent infection, we investigated the ability of pulmonary macrophages (PuM) to phagocytize C. neoformans and produce monocyte chemotactic protein 1 (MCP-1) as a function of the length of time of infection and opsonin. The ability of macrophages to affect serum-mediated phagocytosis varied over the course of infection and was dependent on CD11b/c and CD18 expression. Infection resulted in increased MCP-1 levels within the lung, though the actual amounts varied over the course of infection. Immunohistochemical studies localized MCP-1 expression to macrophages and epithelioid cells. Enhanced production of MCP-1 by PuM from infected rats was confirmed by ex vivo studies. Induction of MCP-1 following serum-mediated phagocytosis was observed for PuM from both infected and noninfected rats and depended on the interaction of C. neoformans with CD11b/c and CD18. Specific antibody was more efficient than serum in promoting phagocytosis and consistently elicited more MCP-1. The relative amount of MCP-1 produced in association with phagocytosis was similar for PuM at all lengths of time of infection. Decreased MCP-1 production was observed for PuM obtained from older rats, including long-term (8 to 10 months)-infected and age-matched controls, suggesting that aging may affect the production of MCP-1 by PuM in response to cryptococcal infection. In summary, our results show that macrophages are an important source of MCP-1 during pulmonary cryptococcosis and that MCP-1 production is actively regulated during infection. Furthermore, we find that phagocytosis of C. neoformans can serve as an important stimulus for MCP-1 production by PuM, though the efficiency of this process is dependent on the opsonin type and may be affected by aging.

Animals↗
PubMed2005

Opsonic requirements for dendritic cell-mediated responses to Cryptococcus neoformans.

The encapsulated pathogenic yeast Cryptococcus neoformans is poorly recognized by phagocytic cells in the absence of opsonins. Macrophages will bind and internalize complement- or antibody-opsonized C. neoformans; however, less is known about the role of opsonins in dendritic cell (DC)-mediated recognition of the organism. Thus, we studied the opsonic requirements for binding to C. neoformans by cultured human monocyte-derived and murine bone marrow-derived DCs and whether binding leads to antifungal activity and cytokine release. Binding of unopsonized C. neoformans to human and murine DCs was negligible. Opsonization with pooled human serum (PHS) increased binding, while heat treatment of PHS virtually abolished this binding, thus suggesting a role for heat-labile complement components. PHS plus a monoclonal anticapsular antibody, 3C2, had an additive effect on binding for most cryptococcal strains. Human and murine DCs exhibited pronounced anticryptococcal activity in the presence of the antibody at early (2-h) and late (24-h) time points; however, PHS opsonization did not supplement this anticryptococcal activity. Antifungal activity against C. neoformans opsonized in PHS and/or antibody was partially reduced in the presence of inhibitors of the respiratory burst response. Human, but not murine, DCs released modest amounts of tumor necrosis factor alpha when stimulated with C. neoformans opsonized in PHS and/or antibody. However, opsonized C. neoformans failed to stimulate detectable release of interleukin 10 (IL-10) or IL-12p70 from either DC population. Thus, human and murine DCs show maximal binding to and antifungal activity against C. neoformans via a process highly dependent on opsonization.

Animals↗
PubMed1989

Ingestion and killing of Listeria monocytogenes by blood and milk phagocytes from mastitic and normal cattle.

Human listeriosis resulting from consumption of listeria-contaminated dairy products is emerging as a significant public health concern. There is a need to understand better the processes involved in the pathogenesis of Listeria monocytogenes-induced bovine mastitis. In the present report, we describe the results of the in vitro interaction of L. monocytogenes with bovine blood and milk leukocytes. Induction of an experimental L. monocytogenes mastitis resulted in a rapid and dramatic increase in neutrophils in the milk of infected cows. Blood neutrophils and mononuclear cells and milk leukocytes from listeria-infected and uninfected cows readily ingested L. monocytogenes in the presence of serum opsonins. These leukocytes also killed a portion of the ingested listeriae. Ingestion of listeriae evoked a vigorous chemiluminescence response by blood neutrophils and a relatively weak response by blood mononuclear cells. Ingestion, killing, and chemiluminescence by milk leukocytes were directly related to the percentage of neutrophils that were present. Blood neutrophils from healthy donor cattle ingested and killed L. monocytogenes when leukocyte-depleted milk and whey from mastitic cows were the sole sources of opsonins, although fewer listeriae were ingested than when normal bovine serum was present. These results indicate that bovine blood and milk phagocytes, like blood and inflammatory phagocytes from other mammalian species, can ingest and kill L. monocytogenes in vitro.

Animals↗
PubMed1990

Heat stability of protective antigen of Leptospira interrogans serovar lai.

Protective antigen (PAg; glycolipid antigen; molecular size, 23 to 30 kilodaltons), the serogroup-specific antigen partially purified from leptospiral cells, is one of the most important protective antigens. The heat stability of PAg was compared with that of whole-cell (WC) antigen by using sodium dodecyl sulfate-polyacrylamide gel electrophoresis, immunoblotting, protective activity, opsonin-inducing activity, agglutinating antibody-inducing activity, and an inhibition test in an enzyme-linked immunosorbent assay. A band of 23 to 30 kilodaltons of PAg, which was seen in untreated PAg and WC, shifted to a position with a molecular size of ca. 20 kilodaltons after heat treatment of PAg at 80 degrees C for 30 min and WC at 100 degrees C for 30 min. In the enzyme-linked immunosorbent assay inhibition test with monoclonal antibody LW2 and a sonicated antigen of WC, the inhibition rate of PAg and WC to sonicated WC was reduced by heat treatment at 80 degrees C for 30 min and at 100 degrees C for 30 min, respectively. Agglutinating antibody-inducing activities and opsonin-inducing activities of PAg and WC in mice were reduced by heat treatment under the same conditions; these activities were assayed by a microscopic agglutination test and by chemical luminescence response in serum from immunized mice, respectively. Protective activity of heated PAg and heated WC in cyclophosphamide-pretreated mice agreed with the results of immunogenicity in mice. These results indicate that the Leptospira PAg is one of the important protective antigens and is altered by heat treatment at 80 degrees C. Furthermore, the immunogenicity and antigenicity of the PAg present in WC are more stable than that of the extracted PAg, and the coexistence of other cellular components with PAg might protect and stabilize PAg from the heat treatment.

Agglutination Tests↗