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Biomedical subjects

A Ljungh

Publications and source records attributed to A Ljungh.

At least 55 records · Page 3Linked to original sources
PubMed1997

Vitronectin-binding staphylococci enhance surface-associated complement activation.

Coagulase-negative staphylococci are well recognized in medical device-associated infections. Complement activation is known to occur at the biomaterial surface, resulting in unspecific inflammation around the biomaterial. The human serum protein vitronectin (Vn), a potent inhibitor of complement activation by formation of an inactive terminal complement complex, adsorbs to biomaterial surfaces in contact with blood. In this report, we discuss the possibility that surface-immobilized Vn inhibits complement activation and the effect of Vn-binding staphylococci on complement activation on surfaces precoated with Vn. The extent of complement activation was measured with a rabbit anti-human C3c antibody and a mouse anti-human C9 antibody, raised against the neoepitope of C9. Our data show that Vn immobilized on a biomaterial surface retains its ability to inhibit complement activation. The additive complement activation-inhibitory effect of Vn on a heparinized surface is very small. In the presence of Vn-binding strain, Staphylococcus hemolyticus SM131, complement activation on a surface precoated with Vn occurred as it did in the absence of Vn precoating. For S. epidermidis 3380, which does not express binding of Vn, complement activation on a Vn-precoated surface was significantly decreased. The results could be repeated on heparinized surfaces. These data suggest that Vn adsorbed to a biomaterial surface may serve to protect against surface-associated complement activation. Furthermore, Vn-binding staphylococcal cells may enhance surface-associated complement activation by blocking the inhibitory effect of preadsorbed Vn.

Animals↗
PubMed1997

Immunoblot assay for serodiagnosis of Helicobacter pylori infections.

An immunoblot assay for the serological diagnosis of Helicobacter pylori infection was evaluated. Serum samples from patients whose gastric biopsy specimens were known to be positive or negative for H. pylori on culture were used to establish interpretive criteria for the immunoblot assay. A panel of sera from patients with diseases other than H. pylori infection and sera from healthy blood donors were included to validate these criteria. All sera were initially assessed in an enzyme immunoassay (Ge-EIA), based on acid glycine-extracted cell surface proteins of H. pylori NCTC 11637. The same antigen extract was used in the immunoblot assay. In addition, the Ge-EIA and the immunoblot assay were compared with a commercially available EIA (Seradyn, Color Vue Pylori). Bands of 110/120 kDa and/or two of five low-molecular-mass proteins (26, 29, 30, 31, and 33 kDa, in any combination) showed a strong correlation with the H. pylori culture-positive patients (97.5%) compared to the correlation obtained with the EIA results (Ge-EIA, 87.5%; Seradyn EIA, 92.5%), and the antibody responses to these proteins were considered specific reactions. In 37 of 40 serum samples from culture-negative patients and also in sera from patients with other disorders, a moderate antibody reactivity to the medium-size proteins (43 to 66 kDa) was observed, and these were considered not valuable for a specific immunoblot assay. Among sera from culture-positive patients, 39 of 40 serum samples were defined to be immunoblot positive, and from among sera from culture-negative patients, 3 of 40 serum samples were defined to be immunoblot positive. The use of sera from patients with negative cultures for H. pylori as negative controls may decrease the sensitivity due to sampling error and false-negative culture results. Immunoblot assay-positive results were detected among 10% of sera from patients with other diseases, whereas they were detected among 42.5% of sera by the Ge-EIA and 47.5% of sera by the Seradyn-EIA. The higher number of EIA-positive sera in this group reflects a possible cross-reactivity (false-positive EIA result). Of the blood donors, representing asymptomatic but possibly colonized subjects, 24% were immunoblot positive. In conclusion, our data indicate that immunoblotting is more sensitive as well as more specific than EIA. Moreover, it permits detection of antibody responses to specific antigens, e.g., the cytotoxin-associated CagA protein, which may have pathological implications.

Adult↗
PubMed1997

Altered immune response to staphylococcal antigens in long-lasting implanted mice.

Staphylococcal infections constitute one of the main problems associated with clinical applications of various prosthetic medical devices (biomaterials). As the magnitude of the infection risk depends often on the duration of device installation, and the incidence of infections is higher in skin-penetrating devices, we studied some parameters of specific immune response to staphylococcal antigens in mice subcutaneously (s.c.) implanted for three months with heparinized polyethylene (H-PE). Three weeks before the evaluation of immune response, mice (implanted and non-implanted) were s.c. infected with 10(7) of Staphylococcus aureus Cowan 1. The proliferation of lymph node cells was determined on the basis of 3H-thymidine incorporation in 3-days cultures stimulated with: staphylococcal lipoteichoic acid (LTA), protein A (SpA), alpha-toxin, or with phytohemagglutinin (PHA). Moreover, the levels of specific antibodies to staphylococcal antigens were determined in serum samples (ELISA against: LTA, SpA, alpha-toxin). The data obtained indicate that long-lasting implantation caused evident changes in proliferative activity of lymphocytes and humoral response to staphylococcal antigens. It enhances alpha-toxin and LTA stimulated proliferation of lymph node lymphocytes in vitro. In contrast, H-PE-implanted animals demonstrated a significant decrease in the production of anti-SpA IgG2a and IgG2b and increase in the synthesis of anti-LTA IgG1 antibodies.

Animals↗
PubMed1996

Protein adsorption and bacterial adhesion to biliary stent materials.

Four biliary stents inserted for relief of jaundice in patients with biliary obstruction due to carcinoma of pancreatic head were examined for the adsorption of biliary proteins and bacterial colonization. Fibronectin and vitronectin (S-protein) were found to be the two main proteins adsorbed on the inner surface of the stents. Biliary isolates included Escherichia coli, Enterococcus faecalis, and Candida albicans. In vitro studies were performed to clarify the kinetics of biliary protein and bacterial adhesion. Biliary drains of polytetrafluorethylene, polyethylene, polyurethane, and rubber were placed in a flow cell and perfused with human bile at 37% C for 24 hr. The materials were subjected to either detection of adsorbed biliary proteins or perfusion with 3 H-labeled E. coli cells (1 X 10 6 cfu/ml). The results show that the adsorbed biliary proteins were detectable on the surface of biliary stents and able to enhance bacterial adhesion to the surface in the first 24 hrs after the exposure of stent materials to bile, and that both the adsorption of biliary proteins and the adhesion of bacterial cells were material- and strain-dependent. Furthermore, there was a clear correlation between the amount of adsorbed fibronectin and the number of adherent bacteria. The results indicate that, in the clinical situation, biliary proteins may be adsorbed on the surface of inserted stents within a short time after insertion, and some of them may be used by bacterial cells as receptors for adhesion to the surface, and thus involved in the process of bacterial adhesion.

Adsorption↗
PubMed1996

Staphylococci bind heparin-binding host growth factors.

Staphylococcus aureus, which mediated binding to heparan sulfate, and also strains of coagulase-negative staphylococci (CNS) adhered in high numbers to polymers with end-point attached heparin. A characteristic feature of several cell growth factors is strong affinity for heparin. In the present study, binding of the 125I-labeled heparin-binding growth factors (HBGF), acidic and basic fibroblast growth factor (aFGF, bFGF), and platelet-derived growth factor (PDGF) by S. aureus and CNS strains was examined. Staphylococcal strains used in this study bind bFGF and PDGF, but not aFGF. The binding of bFGF and PDGF was time dependent, influenced by pH and ionic strength for S. aureus Cowan 1. Preincubation of staphylococcal cells with unlabeled bFGF enhanced bFGF binding, but heparin, protamine sulfate, poly-L-lysine, and suramin were potent inhibitors of 125I-bFGF binding to cells of S. aureus Cowan 1. Glycosaminoglycans of comparable size (chondroitin sulfate), other polysulfated polymers (lambda-carrageenan, fucoidan), and some polysulfated polysaccharides (dextran sulfate, pentosan polysulfate) inhibited binding of both GFs to various extents. The partial inhibition of binding of both GFs after protease and periodate treatments indicates that both proteinaceous and other carbohydrate moieties participate in the binding. A lysozyme cell surface extract and bacterial lysates of S. aureus Cowan 1 competitively inhibited binding of 125I-bFGF and 125I-PDGF. These results suggest that staphylococci have the ability to bind two of the HBGFs, bFGF and PDGF, but not aFGF, via more than one cell structure. These binding structures seem to be exposed on the cell surface and deeply anchored in the cytoplasmic membrane as well.

Anti-Bacterial Agents↗
PubMed1996

Stillbirths and intrauterine infection, histologic chorioamnionitis and microbiological findings.

OBJECTIVE: To analyze whether placental inflammation is associated with stillbirth in Zimbabwe. METHOD: Placentas from 66 stillbirths (> 22 weeks' gestation; patients with congenital malformations, diabetes or preeclampsia were excluded) and 66 term live births were studied for the presence and severity of chorioamnionitis. The morphological results were compared with earlier presented microbiological findings in the same material. RESULTS: Chorioamnionitis was present in 79% of stillbirths and 30% of live births (O.R. 8.5, 95% C.I. 4.0-18). Nine percent of stillbirths but no live births presented vasculitis of the chorionic plate, which verified an inflammatory response from the infant (O.R. 14, 95% C.I. 2.8-72). The same types of microorganisms were isolated from stillbirths and liveborns, but Escherichia coli and group B streptococci were more frequent among stillbirths. CONCLUSIONS: Morphological chorioamnionitis occurred 2.6 times more often in women with stillbirths than in women with live births. In 9% of stillbirths the infant showed an inflammatory response. Thus the infant was alive when the infection occurred and it is therefore reasonable to assume that infection was the cause of death.

Cause of Death↗
PubMed1996

The cells of monocyte-macrophage lineage in mice with the 2-month polyethylene implantation.

End-point-attached heparinized polyethylene (H-PE) was implanted for 2 months into the peritoneum of C57B1/6 mice. The proliferation of bone marrow cells (BMCs) from implanted and non-implanted mice was investigated in M-CSF supplemented medium, in the presence or absence of macrophage-specific monoclonal antibodies (mAbs). The mAb HC 7.67.B, recognizing a surface determinant on immature monocytoid cells, inhibited the proliferation of BMCs from H-PE implanted mice without any influence on the proliferation of BMCs from non-implanted animals. The peritoneal macrophages from H-PE implanted mice demonstrated enhanced production of fibronectin (Fn) in comparison to the macrophages from non-implanted animals. Our results suggest changes in the differentiation of murine monocyte-macrophage lineage in the mice bearing H-PE implants for 2 months.

Animals↗
PubMed1996

The proliferation of human T lymphocytes stimulated by Helicobacter pylori antigens.

Fractionated mononuclear cells (MNCs) were obtained from peripheral blood of healthy human volunteers, seronegative for H. pylori antibodies. The MNCs were stimulated in culture with whole live or heat-killed H. pylori cells or with bacterial cell surface (SA) or cytoplasmic (CA) antigens. There was a marked proliferative response of T cells in cultures stimulated with 10(5) cells/well of live H. pylori, 5 micrograms/well of CA or 5-20 micrograms/well of SA. However, no proliferation was observed in MNC cultures containing higher "doses" of live H. pylori organisms (10(7)/well) or CA (20 micrograms/well). Moreover, higher "doses" of the bacteria or CA entirely inhibited the response of T cells to PHA.

Adhesins, Bacterial↗
PubMed1996

Phagocytosis of Helicobacter pylori bacteria differing in the heparan sulfate binding by human polymorphonuclear leukocytes.

Heparan sulfate binding proteins (HSBPs) of Helicobacter pylori facilitate bacterial phagocytosis by human polymorphonuclear leukocytes (PMNs). H. pylori 25 strain which demonstrates a strong heparan sulfate binding activity was found to be attached to/ingested by PMNs in greater numbers than H. pylori strain 17874 bacteria which lacked this activity. Moreover, heparin inhibited the uptake of cells of H. pylori strain 25 but not of cells of H. pylori strain 17874 by PMNs.

Bacterial Adhesion↗
PubMed1996

A particle agglutination assay for rapid identification of heparin binding to coagulase-negative staphylococci.

The heparin-binding properties of six different species of coagulase-negative staphylococci were examined by a particle agglutination assay. Heparin (mol. wt 4000-6000), mildly treated with sodium periodate, was covalently coupled to amino-modified latex beads (0.72 micron diameter). The particle agglutination assay was validated by comparing results with the adhesion (percentage binding of adherent cells) of coagulase-negative staphylococcal strains to heparinised microtitration plates. Of 38 different coagulase-negative staphylococcal strains tested, 30 showed agglutination reactivity with heparin-coated latex beads. Strains of different coagulase-negative staphylococcal species agglutinated heparin-coated latex beads to various extents (e.g., cells of Staphylococcus haemolyticus strains reacted more strongly than cells of S. epidermidis strains). The agglutination reaction was significantly inhibited by fucoidan, suramin, lambda-carrageenan and other sulphated compounds, but not by non-sulphated carbohydrate polymers such as hyaluronic acid. Agglutination of staphylococcal cells with heparin-coated latex beads was completely blocked by a cell-surface extract. These results suggest that structures responsible for heparin binding are exposed on the cell surface.

Agglutination Tests↗
PubMed1996

Effects of granulocyte-macrophage colony stimulating factor (GM-CSF) on biomaterial-associated staphylococcal infection in mice.

Staphylococcal infections are a major complication in the usage of biomaterials. Different modifications of polymers have been made to reduce the incidence of such infections. We studied the effects of modifying heparinized polyethylene (H-PE) with mouse recombinant granulocyte-macrophage stimulating factor (rGM-CSF). The elimination of staphylococci (Staphylococcus aureus, S. epidermidis) from the peritoneum of mice implanted with rGM-CSF-coated H-PE was slightly more effective than the elimination of the bacteria from the peritoneum of animals implanted with uncoated H-PE. Most interestingly, the number of staphylococci present in the biofilms covering rGM-CSF-coated implants were significantly lower than the number of bacteria detected on the surface of H-PE not coated with rGM-CSF. In vitro, rGM-CSF restored the anti-bacterial potency of the phagocytes, which had been reduced by surface contact with H-PE. The results suggest that modification of biomaterials with rGM-CSF could be one way of preventing staphylococcal infections; especially in neutropenic disorders, which constitute the highest risk factor for foreign body-associated infections.

Animals↗
PubMed1996

Invasion of tissue culture cells by diarrhoeagenic strains of Escherichia coli which lack the enteroinvasive inv gene.

Invasive Escherichia coli strains of certain serotypes invade by the same mechanism as the Shigella sp. It has been proposed that invasion of epithelial cells by EPEC strains may also occur; this is a previously overlooked property. In the present study E. coli strains isolated from patients with diarrhoea or ulcerative colitis, lacking the inv plasmid mediating classical invasion, but hybridizing with probes for different adhesins, were analyzed for their ability to invade HeLa and Caco-2 cells. The majority of strains invaded Caco-2 cells to a higher extent than HeLa cells. Adhesion to Caco-2 cells was a prerequisite for subsequent invasion of the cells but EAF, eae, EAgg and other known virulence factors were not sufficient to mediate invasion. In 8/9 E. coli strains invasion was enhanced after growth under iron restriction. Growth during anaerobic conditions did not influence subsequent invasion by E. coli strains whereas 6/9 strains had their invasive ability significantly decreased after growth in the presence of 1% glucose. The invasive process was inhibited by mannose but not by lactose, fucose or galactose. Our data indicate that strains of E. coli may invade Caco-2 cells by novel mechanisms which require adhesion to the cells but which differ from those of Salmonella sp., Yersinia sp., Shigella sp. and classical enteroinvasive E. coli.

Adhesins, Bacterial↗
PubMed1996

Syphilis seroprevalence among pregnant women and its role as a risk factor for stillbirth in Maputo, Mozambique.

OBJECTIVE: To elucidate the role of current syphilis as a risk factor for foetal death. METHODS: Sera were obtained from 57 women with third trimester foetal death (cases) and 58 women with foetus alive (controls) matched for age and parity. All sera reactive in qualitative Rapid Plasma Reagin (RPR) analyses were tested with serial twofold dilutions to determine endpoint flocculation titres and tested with the micro-haemagglutination assay for Treponema pallidum (MHA-TP). Placental biopsies were sectioned and stained by haematoxylin-eosin and Warthin-Starry for light microscopy. SETTING: Central Hospital, in Maputo, Mozambique, from January 1990 to June 1991. RESULTS: The MHA-TP was reactive in 42% of cases and in 12% of controls (OR = 5.3; 95% CI: 1.9-15.4). The RPR card test was reactive at the dilution of 1.32 or greater in 28% of cases and in 7% of controls. All these results were confirmed by MHA-TP (OR = 5.3; 95% CI: 1.5-15.4). In 9/28 (32%) MHA-TP seroreactive women (7 cases and 2 controls) placental morphological changes indicated syphilitic infection. CONCLUSION: MHA-TP seroreactivity and high titre RPR were associated with stillbirth. Morphological changes presumptive of syphilis infection were found in 32% placentas histologically studied. Syphilis is a risk factor for foetal death in Maputo, Mozambique.

Case-Control Studies↗
PubMed1996

A bacteriologic and scanning electron microscope study after implantation of foreign bodies in the biliary tract in rats.

BACKGROUND: Bacterial adherence to the stent surfaces, concomitant colonization, and possible stent blockage are the main complications after the use of biliary stents. The present study was assigned to investigate bacteriologic and morphologic changes in the biliary tract after the implantation of biliary drain materials. METHODS: Rubber and silicone pieces with a surface area of 1 cm2 were implanted into the biliary tract in rats after temporary obstruction of the common bile duct by the use of a mini-occluder. The animals were killed at 4, 8 and 14 weeks, respectively, after implantation, and the implants were retrieved, cultured, and examined by scanning electron microscopy (SEM). Bacterial culture and SEM were also performed on tissue samples obtained from the mucosal surface of the biliary tract. RESULTS: Bacterial colonization and biofilm formation were found on the surfaces of the implanted materials and on the mucosal surface of the biliary tract in animals with implants but not on the biliary tract mucosa in rats without implants. CONCLUSION: Foreign bodies implanted in the biliary tract facilitate bacterial adherence not only to the surface of the implants but also to the mucosal surface in the biliary tract.

Animals↗