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T Wadström

Publications and source records attributed to T Wadström.

At least 109 records · Page 6Linked to original sources
PubMed1995

Cell-surface charge and cell-surface hydrophobicity of collagen-binding Aeromonas and Vibrio strains.

Partitioning in aqueous polymer two-phase systems of polyethylene glycol and dextran was used to detect and compare cell-surface charge and cell-surface hydrophobicity of Aeromonas hydrophila, A. caviae, A. sobria, Vibrio cholerae, and V. anguillarum strains. These strains have cell-surface components that bound either native or thermally denatured type I collagen (i.e., a mixture of the alpha1+alpha2 chains) and gelatin immobilized on latex beads. Our goals were: (1) to compare the possible relationship between the cell-surface charge/hydrophobicity and binding to collagen and (2) to evaluate the influence of the culture media on the expression of surface properties. There was no apparent relationship between cell-surface charge, cell-surface hydrophobicity, and binding to collagen. The expression of surface properties was dependent on the culture media. There was no relationship between binding to immobilized collagen and binding to soluble 125I-labeled collagen. Particle-agglutination reactivity differed when using various collagen-coated microbead preparations. There were general differences in the particle-agglutination reactivity when collagen-coated latex beads were prepared using different coating procedures. The negative charge and hydrophobicity of the various collagen-coated microbead preparations were also studied by partitioning in the two-phase system of polyethylene glycol and dextran. Under these conditions, the alpha1+alpha2 collagen-chain mixture covalently immobilized on carboxy-modified latex beads was less hydrophobic and negatively charged than gelatin and native collagen immobilized on the same kind of latex beads. For latex beads passively coated with collagen preparations, the alpha1+alpha2 collagen-chain mixture was more hydrophobic than gelatin and native collagen. We suggest that for screening collagen-binding among Vibrio and Aeromonas strains, a reliable and sensitive particle-agglutination assay should consider the collagen preparation and the coating procedure for the immobilization of collagen onto the latex beads. In this regard, carboxy-modified latex beads coated with an alpha1+alpha2 collagen-chain mixture gave the best results.

Aeromonas↗
PubMed1995

Helicobacter pylori infection and foreign travel.

Seroprevalence of antibodies to Helicobacter pylori is generally higher in developing than in developed countries. The route of transmission of H. pylori is unknown but is most commonly assumed to be fecal-oral. Gastroenteritis in a person traveling to developing countries is often a marker of exposure to fecally contaminated food or water. Of 133 initially seronegative young Swedes traveling to developing countries for a total of 16.4 years, of whom 102 reported having had at least one episode of gastroenteritis, not one seroconverted. This rate is lower than in studies of residents in developed countries and casts some doubt on the theory of fecal-oral transmission via a common source as an important mode of transmission of infection with Helicobacter pylori.

Adolescent↗
PubMed1995

Antibody response to Staphylococcus aureus collagen binding protein in patients with S. aureus septicaemia and collagen binding properties of corresponding strains.

An ELISA was developed for the detection of IgG antibodies to Staphylococcus aureus collagen binding protein (CnBP) in 95 patients with S. aureus endocarditis, complicated septicaemia with bone and joint involvement or uncomplicated septicaemia and in 95 control patients. Sixty percent of S. aureus-infected patients showed a positive peak anti-CnBP antibody level or a significant rise in titre, or both, during infection, but patients with S. aureus endocarditis or complicated septicaemia could not be differentiated from those with uncomplicated S. aureus septicaemia. The collagen binding capacity of S. aureus strains from 82 of the 95 patients was investigated in a particle agglutination assay and a 125I-labelled assay. All strains bound collagen in the particle agglutination assay as did 68% in the 125I-labelled assay, but there was no correlation between collagen binding of the patient strain and endocarditis, joint or skeletal involvement. An anti-CnBP antibody response was seen in 16 patients infected with a S. aureus strain negative for collagen binding in vitro, indicating in-vivo expression of CnBP.

Adolescent↗
PubMed1995

Growth conditions influence expression of cell surface hydrophobicity of staphylococci and other wound infection pathogens.

The initial adhesion of microbes to tissue and solid surfaces can be mediated by hydrophobic interaction. Expression of microbial cell surface hydrophobicity (CSH) is influenced by growth conditions, and often best expressed after growth under nutrient-poor conditions, or "starvation". In the present study, the CSH of 133 strains of Enterobacteriaceae, Staphylococcus aureus, coagulase-negative staphylococci, Enterococcus faecalis, group A streptococcus, Pseudomonas aeruginosa, Clostridium perfringens, Bacteroides fragilis, Peptococcus magnus, and of 8 Candida albicans strains was measured by the salt aggregation test after growth on hematin agar in a 5% CO2 atmosphere, or under anaerobiosis. Cells of all but 8 strains expressed pronounced or moderate CSH, i.e., they aggregated in 0.01-2 M ammonium sulfate. When the agar surface was covered by human serum (diluted 1:5) to mimic growth conditions in a wound, 94 strains expressed higher CSH, and 44 strains the same CSH as after growth without serum. The CSH of 12 strains of different species was measured after growth on blood, hematin and PDM agar, with or without serum, and in an aerobic or a 5% CO2 atmosphere. The highest CSH was expressed after growth in 5% CO2 with serum, and the lowest growth after on blood agar in aerobic atmosphere. Identical results were obtained with native and heat-inactivated (56 C, 20 min) serum. The reduced surface tension obtained in 5% CO2, as well as yet unidentified serum factors, promotes expression of CSH.

Bacterial Adhesion↗
PubMed1995

Attachment, ingestion and intracellular killing of Helicobacter pylori by human peripheral blood mononuclear leukocytes and mouse peritoneal inflammatory macrophages.

The different steps of phagocytosis, attachment, ingestion and intracellular killing of cells of Helicobacter pylori strain 17874 (expressing sialic acid-specific haemagglutinin) and cells of H. pylori strain 17875 (expressing non-sialic acid-specific haemagglutinin) have been studied. More cells of sialopositive H. pylori strain 17874 have been found attached to human peripheral blood mononuclear leukocytes (PBM) and mouse peritoneal inflammatory macrophages (PIM) than cells of sialonegative H. pylori strain 17875. Binding of cells of H. pylori strain 17874 has been significantly inhibited by treatment of phagocytes with neuraminidase. Inhibition of adhesion of these bacteria preincubated with foetuin to normal phagocytic cells has also been found. Well adhering cells of H. pylori strain 17874 were more resistant to killing mechanisms of human PBM and mouse PIM than cells of strain 17875. Good, probably sialic acid-specific haemagglutinin dependent, adhesion of H. pylori bacteria to phagocytes can be considered as an important virulence factor which facilitates the pathogen to avoid the defence mechanisms.

Animals↗
PubMed1995

Association of Helicobacter pylori and gastric autoimmunity: a population-based study.

Based on clinical studies, a negative association between Helicobacter pylori and autoimmune corpus gastritis is described. In the present investigation of an unselected population of 1461 adults we can state, however, that there exists a relationship between H. pylori infection and the development of gastric corpus autoimmunity. As confirmation for the gastric autoantibody development through molecular mimicry, a high homology (72% in 25 amino acid overlap) between the beta subunit of H. pylori urease and that of H + K + ATPase, the gastric parietal cell autoantigen, was revealed.

Adolescent↗
PubMed1995

Immunological properties of the cell surface haemagglutinins (sHAs) of Helicobacter pylori strain NCTC 11637.

Rabbits were immunised with stage 1 and stage 2 soluble haemagglutinins (sHA) of Helicobacter pylori strain NCTC 11637 and with rabbit erythrocytes coated with stage 1 sHA. After adsorption of stage 1 sHA on erythrocytes, SDS-PAGE analysis showed that 4 major protein bands were removed from the preparation. The anti-sHA coated erythrocyte serum had the highest HA inhibition titre of 16. Crossed immunoelectrophoresis of the stage 1 sHA, against stage 1 and 2 antisera showed multiple precipitin arcs; however, the anti-sHA coated erythrocyte serum produced only two arcs. One arc produced by the anti-stage 2 serum was absent with the anti-stage 1 serum. This arc could have been produced against a 20 kDa polypeptide which was absent in the stage 1 sHA. The other arc was stronger when compared with that produced by anti-stage 1 serum. These two arcs corresponded to the two arcs produced by the anti-sHA coated erythrocyte serum, which had the highest inhibition titre. The two arcs were markedly reduced in crossed immunoelectrophoresis with an adsorbed stage 1 sHA preparation, which indicates that these arcs were produced against the sHAs.

Animals↗
PubMed1995

Helicobacter pylori interacts with heparin and heparin-dependent growth factors.

The pathogenic bacterium Helicobacter pylori, which causes active, chronic type B gastritis and peptic ulcer disease, and increases the risk for development of gastric cancer, could tentatively interfere with growth factors and growth factor receptors of importance for the gastroduodenal mucosa, e.g. heparin-binding FGFs (fibroblast growth factors). H. pylori binds FGF with an extremely strong affinity (3.8 x 10(-12)M), and also heparan sulfate and heparin with higher affinity (Kd 9 x 10(-9)M) than FGFs bind to heparin (10(-8) - 10(-9)M). FGF receptors are also dependent on heparin for their activation. Heparan sulfate binding proteins (HSBP) are exposed on and shed from the surface of H. pylori, which often are localised close to the epithelial stem cells in the gastroduodenal glands. H. pylori could thus efficiently interfere with growth factors and growth factor receptors, tentatively resulting in disturbance of the delicate balance that control the renewal, maintenance and repair of the gastroduodenal mucosa. This mode of action has previously not been considered, but may constitute part of its pathogenic mechanisms. Such a dynamic mode of action of H. pylori may explain the reason for that infected victims may either suffer from gastrointestinal symptoms or lack clinical evidence of disease or discomfort.

Fibroblast Growth Factor 1↗
PubMed1995

The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages.

The aim of this study was to determine the role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages. Two H. pylori strains expressing sialic acid-specific haemagglutinins but differing in the expression of heparan sulphate-binding capacity were chosen for investigation. The attachment to an ingestion by macrophages of the H. pylori bacteria were estimated by ELISA using anti-H. pylori antibodies. The adhesion of both H. pylori strains could be inhibited by pretreatment of the bacteria with heparin (H), HS or fetuin, as well as by preincubation of the macrophages with heparinase or neuraminidase. However, detailed analysis of the data on the inhibition of bacterial adhesion to macrophages led to the conclusion that the attachment of H. pylori 25 bacteria, which expressed a high heparan sulphate binding, was mainly determined by HS-binding structures. In contrast, the adhesion to macrophages of H. pylori bacteria 17874 microbes, which expressed a weak heparan sulphate binding, was more dependent on the exhibition of sialic acid-dependent haemagglutinins. The described variation in H. pylori bacterial surface structures mediating their adhesion to macrophages could suggest a similar variation in bacterial adhesion to stomach mucosa and maybe in the pathogenicity of H. pylori strains.

Animals↗
PubMed1995

Phenotypic characterization of epidemic versus sporadic strains of methicillin-resistant Staphylococcus aureus.

Forty strains of methicillin-resistant Staphylococcus aureus (MRSA) were divided on the basis of their epidemiologic behavior into two subgroups, sporadic MRSA (SMRSA) and epidemic MRSA (EMRSA) strains. The strains were examined for binding of 125I-labelled fibronectin, vitronectin, collagen, Fc fragments of immunoglobulin G, and fibrinogen. A significant difference between EMRSA and SMRSA strains was found for binding of 125I-labelled fibrinogen and for Fc fragments of immunoglobulin G, (P < 0.05). No significant difference in the binding of 125I-labelled fibronectin and collagen was found between EMRSA and SMRSA strains. The binding of 125I-labelled vitronectin to MRSA strains was found to be aspecific. Capsular serotypes of the strains were determined with monoclonal antibodies against capsular types 5 and 8. Strains could be divided into the following four groups: types 5, 8, and 5/8 and nontypeable. More nontypeable strains were found in the EMRSA group (66.6%). Significantly more EMRSA strains (79%) than SMRSA strains (44%) produced alpha-toxin (P < 0.025). Logistic regression analysis using a combination of the parameters 125I-labelled immunoglobulin G binding, capsular type, and alpha-toxin production predicted the epidemic character with a sensitivity of 83% and a specificity of 75%.

Bacterial Toxins↗
PubMed1995

Association of Helicobacter pylori gastric infection with the suppressed Thomsen-Friedenreich antigen natural humoral response.

BACKGROUND: A low natural humoral immune response to Thomsen-Friedenreich antigen (TFA) is a general phenomenon in patients with cancer, including gastric cancer, and in some premalignant conditions. It has been also shown that Helicobacter pylori infection is associated with increased risk of gastric cancer. The possible link between the TFA immune response and H. pylori infection was investigated. METHODS: Enzyme-linked immunosorbent assay with H. pylori cell surface glycine extract as antigen and microhemagglutination of neuraminidase-treated blood group O donor erythrocytes were used for evaluation of IgG H. pylori antibody and TFA agglutinin levels in sera from patients with gastric cancer (n = 39) or ulcer of the stomach (n = 36) and controls (n = 49). RESULTS: The tendency to an inverse relationship between the two events was found in all groups studied, including cancer. H. pylori-seronegative persons had higher TFA natural antibody titer than the related H. pylori-seropositive groups. When log2 of TFA antibody titer > 4 for strong TFA responders and H. pylori relative antibody activity > 25 for H. pylori-seropositive persons were chosen as cut-off limits, the association was statistically significant (p < 0.02). TFA antibody level was decreased in cancer patients as compared with controls (p < 0.002). No relation to age, stage of the disease, or tumor morphology was noted. CONCLUSION: The data suggest that the TFA natural immune response, which is known to participate in tumor-host relationships, is also involved in H. pylori-host interactions, probably as a natural factor of resistance against H. pylori infection.

Antibodies↗
PubMed1995

Helicobacter pylori and acute bleeding peptic ulcer.

OBJECTIVE: The prevalence of Helicobacter pylori in chronic peptic ulcer is well known. In this study the frequency of H. pylori infection was investigated in patients with acute bleeding peptic ulcer. DESIGN AND SETTING: Prospective study in a district hospital. PATIENTS: Seventy consecutive patients with acute bleeding peptic ulcer. INTERVENTIONS: Diagnosis was verified on admission by endoscopy, and healing was examined at follow-up. Previous history of ulcer disease, presence of dyspeptic symptoms and consumption of non-steroidal anti-inflammatory drugs were recorded. MAIN OUTCOME MEASURES: H. pylori infection was detected by two serological tests in samples obtained on admission for the acute bleeding episode, and at follow-up 1-3 months later. RESULTS: With a commercial latex immunoassay, 53% of the patients with gastric ulcer and 62% with duodenal ulcer were shown to possess H. pylori antibodies. In the other test, a standard enzyme-linked immunosorbent assay based on cell surface protein antigens of H. pylori with high sensitivity and specificity, 81% of gastric ulcer patients and 85% of duodenal ulcer patients were shown to have H. pylori antibodies. CONCLUSION: The results indicate that H. pylori infection plays a major aetiological role in patients with acute bleeding peptic ulcer.

Acute Disease↗
PubMed1995

Particle agglutination assay for detection of albumin and IgG binding cell surface components of Helicobacter pylori.

Human serum albumin (HSA), bovine serum albumin (BSA) and human IgG were immobilized on latex beads to detect cell surface components of Helicobacter pylori binding to BSA, HSA, and IgG by a particle agglutination assay (PAA). In a total of 32 H. pylori strains tested, 16 strains interacted with BSA and 12 strains with HSA; 24 strains expressed binding of human IgG. The specificity of the agglutination reaction was studied by a particle agglutination inhibition assay performed by pre-incubating bacterial cell suspensions in buffers containing homologous proteins, unrelated glycoproteins and a number of common monosaccharides. Treatment of H. pylori cells with heat and proteolytic enzymes abolished binding to microbeads with immobilized IgG and albumin. IgG-binding surface components from cells of H. pylori strain CCUG 17875 were effectively extracted by incubating a cell suspension with 10 mM EDTA, 0.015 M sodium phosphate buffer (pH 7.2), and by washing H. pylori cells with distilled water. However, attempts to extract a fraction rich in albumin-binding components were unsuccessful. We conclude that cells of various H. pylori strains express commonly IgG-binding proteins, and that albumin-binding is probably mediated by non-specific hydrophobic interactions.

Antigens, Bacterial↗
PubMed1994

Purification of collagen-binding proteins of Lactobacillus reuteri NCIB 11951.

Collagen type-I-binding proteins of Lactobacillus reuteri NCIB 11951 were purified. The cell surface proteins were affinity purified on collagen Sepharose and eluted with an NaCl gradient. Two protein bands were eluted from the column (29 kDa and 31 kDa), and both bound radio-labeled collagen type I. Rabbit antisera raised against the 29 kDa and 31 kDa protein reacted with the affinity-purified proteins in a Western blot with whole-cell extract used as antigen. The N-terminal sequence of the 29-kDa and 31-kDa proteins demonstrated the closest homologies with internal sequences from an Escherichia coli trigger factor protein (TIG.ECOLI). Out of nine other lactobacilli, the antisera reacted only with the L. reuteri and not with the other species tested.

Amino Acid Isomerases↗