Biomedical subjects

Torkel Wadstrom

Publications and source records attributed to Torkel Wadstrom.

8 recordsLinked to original sources

PubMed2006

Helicobacter species ribosomal DNA in the pancreas, stomach and duodenum of pancreatic cancer patients.

AIM: To determine whether gastric and enteric Helicobacter species are associated with pancreatic cancer. METHODS: Patients with exocrine pancreatic cancer (n = 40), neuroendocrine cancer (n = 14), multiple endocrine neoplasia type 1 (n = 8), and chronic pancreatitis (n = 5) were studied. Other benign pancreatic diseases (n = 10) and specimens of normal pancreas (n = 7) were included as controls. Pancreatic tissue specimens were analyzed by Helicobacter-specific PCR-assay and products were characterized by denaturing gradient electrophoresis and DNA-sequencing. From a subset of the pancreatic cancer patients, gastric and/or duodenal tissue as well as gallbladder and ductus choledochus tissue were analyzed. Gallbladder and choledochus samples were included as controls. Stomach and duodenum samples were investigated to analyze whether a gastric helicobacter might disseminate to the pancreas in pancreatic cancer patients. Pancreatic specimens were analyzed by Bacteroides-specific PCR for detecting the translocation of indigenous gut microbes to the diseased pancreas. RESULTS: Helicobacter DNA was detected in pancreas (tumor and/or surrounding tissue) of 75% of patients with exocrine cancer, 57% of patients with neuroendocrine cancer, 38% of patients with multiple endocrine neoplasia, and 60% of patients with chronic pancreatitis. All samples from other benign pancreatic diseases and normal pancreas were negative. Thirty-three percent of the patients were helicobacter-positive in gastroduodenal specimens. Surprisingly, H. bilis was identified in 60% of the positive gastroduodenal samples. All gallbladder and ductus choledochus specimens were negative for helicobacter. Bacteroides PCR-assay was negative for all pancreatic samples. CONCLUSION: Helicobacter DNA commonly detected in pancreatic cancer suggests a possible role of the emerging pathogens in the development of chronic pancreatitis and pancreatic cancer.

Adult↗

PubMed2005

Probiotics for the developing world.

Every minute of every day more and more children die of diarrheal diseases and women, and girls become infected by HIV. An estimated 7,000 women become infected each day. While many valiant efforts are being made to address these issues, until now they have proved to be markedly ineffective. The notion that lactic acid bacteria, formulated into food or dietary supplements, could have a role to play in slowing the morbidity and mortality associated with HIV/AIDS and gastroenteritis, is built upon sound clinical findings and scientific investigations, yet no international efforts have been placed in this approach, to date. We hereby summarize the reasons why such efforts should be made, provide an example of one model being set up in sub-Saharan Africa, and challenge the international community to consider the potential benefits of probiotics, especially for communities not reached by governmental and nongovernmental agencies.

Developing Countries↗

PubMed2003

Helicobacter pylori lipopolysaccharide in the IL-2 milieu activates lymphocytes from dyspeptic children.

In this study, we assessed the proliferative response of peripheral blood mononuclear leukocytes (PBML) from 33 children/young adolescents with chronic dyspepsia, to H. pylori LPS in the presence and absence of IL-2 as a T cell growth factor. A rapid urease test (RUT) and a presence of Helicobacter-like organisms (HLO) in the biopsy specimens allowed us to distinguish RUT/HLO-positive (17/33) and -negative (16/33) patients. H. pylori LPS alone induced a proliferation of PBML from 4 out of 33 dyspeptic patients. IL-2 increased the prevalence of the response to LPS to 59% and 74% of RUT/HLO-positive and -negative patients, respectively. PBML from RUT/HLO-positive patients responded significantly less intensively to H. pylori LPS in the presence of IL-2, to IL-2 alone and to H. pylori LPS+IL-2. However, there was no difference in PHA-driven proliferation of PBML from the patients of those two groups. A negative correlation between the responsiveness to H. pylori LPS of PBML and occurrence of type B inflammation in gastric mucosa was demonstrated. The results suggest a contribution of H. pylori LPS to an outcome of H. pylori infection. It is speculated that H. pylori LPS by an activation of immunocompetent cells may reduce gastric inflammation, decrease bacterial load and prolong H. pylori infection.

Adolescent↗

PubMed2003

A link between Helicobacter pylori and/or Chlamydia spp. infections and atherosclerosis.

Antibodies to Helicobacter pylori, Chlamydia spp. and Mycobacterium bovis were determined in patients with coronary heart disease, H. pylori-related dyspepsia, and tuberculosis, and healthy controls. Enzyme-linked immunosorbent assay was conducted with a glycine extract and CagA protein of H. pylori, chlamydial lipopolysaccharide and mycobacterial heat shock protein Hsp65. The prevalence of anti-glycine extract IgG in coronary heart disease patients was higher than in the tuberculosis group and controls, and the same as in dyspeptic patients. Anti-chlamydial IgG were more prevalent in the coronary heart disease group than in healthy subjects. There was no difference in the prevalence of anti-CagA IgG in the coronary heart disease group and controls or anti-Hsp65 IgG in the patients with coronary heart disease, dyspepsia, tuberculosis, and controls. Anti-glycine extract IgA (like anti-glycine extract IgG) were more prevalent in the coronary heart disease group than in the healthy group. The highest anti-glycine extract IgG/IgA and anti-chlamydial IgG titers were more frequent in coronary heart disease patients as compared with controls. Infections with H. pylori and Chlamydia spp. and enhanced production of antibodies to these pathogens may predispose to human atherosclerosis.

Adult↗

PubMed2003

Five month persistence of Helicobacter pylori infection in guinea pigs.

Seven Dunkin-Hartley guinea pigs were infected with the Sydney strain of H. pylori (SS1). Gastric histopathology was evaluated and serum antibody response to H. pylori cell-surface proteins was analysed by enzyme immunoassay (EIA) and immunoblot. Tissue and faecal samples from five control animals were analysed for the presence of naturally occurring Helicobacter spp. infection by culture and Helicobacter genus-specific PCR. The H. pylori infection persisted for 5 months, in most animals accompanied by a histologically severe antral gastritis, exhibiting focal degeneration and necrosis of gastric crypt epithelium. Increased numbers of mitotic figures were observed in the gastric epithelium, indicating a regenerative process. Infected animals displayed specific antibodies towards H. pylori cell-surface proteins in immunoblot, whereas EIA was of dubious value creating false-positive results. Serum complement C3 and cholesterol levels appeared to be elevated in infected animals. Helicobacter spp. infection was not detected in the control animals. The persistent infection, accompanied by severe gastritis and a prominent serum antibody response, and the apparent absence of a natural Helicobacter spp. infection makes the guinea pig model useful in H. pylori research.

Animals↗

PubMed2002

Lactotetraosylceramide, a novel glycosphingolipid receptor for Helicobacter pylori, present in human gastric epithelium.

The binding of Helicobacter pylori to glycosphingolipids was examined by binding of (35)S-labeled bacteria to glycosphingolipids on thin-layer chromatograms. In addition to previously reported binding specificities, a selective binding to a non-acid tetraglycosylceramide of human meconium was found. This H. pylori binding glycosphingolipid was isolated and, on the basis of mass spectrometry, proton NMR spectroscopy, and degradation studies, were identified as Galbeta3GlcNAcbeta3Galbeta4Glcbeta1Cer (lactotetraosylceramide). When using non-acid glycosphingolipid preparations from human gastric epithelial cells, an identical binding of H. pylori to the tetraglycosylceramide interval was obtained in one of seven samples. Evidence for the presence of lactotetraosylceramide in the binding-active interval was obtained by proton NMR spectroscopy of intact glycosphingolipids and by gas chromatography-electron ionization mass spectrometry of permethylated tetrasaccharides obtained by ceramide glycanase hydrolysis. The lactotetraosylceramide binding property was detected in 65 of 74 H. pylori isolates (88%). Binding of H. pylori to lactotetraosylceramide on thin-layer chromatograms was inhibited by preincubation with lactotetraose but not with lactose. Removal of the terminal galactose of lactotetraosylceramide by galactosidase hydrolysis abolished the binding as did hydrazinolysis of the acetamido group of the N-acetylglucosamine. Therefore, Galbeta3GlcNAc is an essential part of the binding epitope.

Chromatography, Gas↗

PubMed2000

Agglutination of Helicobacter pylori coccoids by lectins.

AIM:To study the agglutination pattern of Helicobacter pylori coccoid andspiral forms.METHODS:Assays of agglutination and agglu-tination inhibition were applied using fifteen commercial lectins.RESULTS:Strong agglutination was observed with Mannose specific Concanavalin A(Con A), fucose specific Tetragonolobus purpureas(Lotus A) and N-acetyl glucosamine-specific Triticum vulgaris (WGA) lectins. Mannose and fucose specific lectins were reactive with all strains of H. pylori coccoids as compared to the spirals. Specific carbohydrates, glyco-proteins and mucin were shown to inhibit H. pylori lectin agglutination reactions.Pre-treatment of the bacterial cells with formalin and sulphuric acid did not alter the agglutination patterns with lectins. However, sodium periodate treatment of bacterial cells were shown to inhibit agglutination reaction with Con A, Lotus A and WGA lectins. On the contrary, enzymatic treatment of coccoids and spirals did not show marked inhibition of H. pylori-lectin agglutination. Interes-tingly, heating of H. pylori cells at 60° for 1 hour was shown to augment the agglutination with all of the lectins tested.CONCLUSION:The consi-derable differences in lectin agglutination patterns seen among the two different-tiated forms of H. pylori might be attributable to the structural changes during the events of morphological trans-formation, resulting in exposing or masking some of the sugar residues on the cell surface. Possibility of various sugar residues on the cell wall of the coccoids may allow them to bind to different carbohydrate receptors on gastric mucus and epithelial cells. The coccoids with adherence characteristics like the spirals could aid in the pathogenic process of Helicobacter infection. This may probably lead to different clinical outcome of H. pylori associated gastro-duodenal disease.

Journal Article↗

PubMed1999

Glycosaminoglycan-binding microbial proteins in tissue adhesion and invasion: key events in microbial pathogenicity.

Glycosaminoglycans such as heparin, heparan sulphate and dermatan sulphate, are distributed widely in the human body. Several glycosaminoglycans form part of the extracellular matrix and heparan sulphate is expressed on all eukaryotic surfaces. The identification of specific binding to different glycosaminoglycan molecules by bacteria (e.g., Helicobacter pylori, Bordetella pertussis and Chlamydia trachomatis), viruses (e.g., herpes simplex and dengue virus), and protozoa (e.g., Plasmodium and Leishmania), is therefore of great interest. Expression of glycosaminoglycan-binding proteins depends on growth and culture conditions in bacteria, and differs in various phases of parasite development. Glycosaminoglycan-binding microbial proteins may mediate adhesion of microbes to eukaryotic cells, which may be a primary mechanism in mucosal infections, and are also involved in secondary effects such as adhesion to cerebral endothelia in cerebral malaria or to synovial membranes in arthritis caused by Borrelia burgdorferi. It has been suggested that they may enhance intracellular survival in macrophages. Microbial binding of heparin may interfere with heparin-dependent growth factors. Whether or not glycosaminoglycan-binding proteins mediate invasion of epithelial cells is a matter of controversy. Heparin and other glycosaminoglycans may have potential uses as therapeutic agents in microbial infections and could form part of future vaccines against such infections.

Animals↗