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M Nilius

Publications and source records attributed to M Nilius.

14 recordsLinked to original sources
PubMed1999

Imidazoline recognition sites and stomach function.

Radioligand binding experiments carried out in cell membranes from rat and human stomach revealed the existence of non-adrenoceptor [3H]clonidine and [3H]idazoxan binding sites and of [3H]DTG (1,2-di-(2-tolyl)guanidine) binding sites. In rat stomach, specific binding was inhibited by imidazolines and guanidines and by non-imidazoline sigma-site ligands, respectively, at different rank orders of affinity, suggesting the existence of non-I1/non-I2 [3H]clonidine binding sites, I2-imidazoline binding sites as well as sigma 2-like-sites. These sites are not directly related to a postsynaptic contractile effect on rat gastric smooth muscle or to acid release from isolated gastric glands. Finally, we demonstrated that the gastric pathogen Helicobacter pylori is able to form and to release the endogenous imidazoline receptor ligand agmatine and that considerable amounts of agmatine are present in human gastric juice. The quantities of agmatine were higher in gastric juice from H. pylori-positive than H. pylori-negative patients.

Animals↗
PubMed1998

Prevalence of Helicobacter pylori resistance to several antimicrobial agents in a region of Germany.

To evaluate the prevalence of resistance among Helicobacter pylori in Germany, the minimum inhibitory concentrations of amoxicillin, tetracycline, clarithromycin, and metronidazole were determined by means of the E test, for 271 Helicobacter pylori isolates cultured from biopsies taken during routine endoscopies in 1996 and 1997. The prevalence of metronidazole resistance was 32.1%, with resistance found more frequently in women (38.5%) than in men (24.4%). Clarithromycin resistance was rare (3.3%). Eight of nine strains resistant to clarithromycin were also resistant to metronidazole. Resistance to either metronidazole or clarithromycin was significantly (P=0.022) higher in patients with duodenal ulcer. No strain was found to be resistant to amoxicillin or tetracycline.

Adult↗
PubMed1998

Performance of a rapid whole blood test for Helicobacter pylori in primary care: a German multicenter study.

BACKGROUND: Serological rapid whole-blood tests for the detection of H. pylori are presently being promoted for use in primary care. We conducted a multi-center study to investigate the diagnostic accuracy of the Boehringer Mannheim Helicobacter pylori test (BM test), which is identical with the Cortecs Helisal test. PATIENTS AND METHODS: A previous diagnosis of H. pylori, a history of peptic ulcer diseases, or proton-pump inhibitor, bismuth or antibiotic use during the preceding month were exclusion criteria. The BM test was performed prior to endoscopy by 7 primary care physicians, 5 practicing gastroenterologists, or a single physician in the university hospital outpatient service. During endoscopy, antral and corpus biopsies were obtained for histology and rapid urease testing (RUT). H. pylori positivity was defined by histology and/or RUT as reference methods. H. pylori IgG-ELISA was performed additionally. RESULTS: Of the 203 patients included, 151 were H. pylori-positive by reference methods (74.4%). The overall accuracy of the BM test was 77.3%. Eight BM tests were indeterminate, and in the other 195 patients the test performed as follows: sensitivity 80.3%, specificity 81.3%, positive predictive value 92.9%, negative predictive value 57.4%. Using IgG-ELISA as reference, the BM test performance was similar. It also did not differ substantially among the three groups of physicians involved. CONCLUSIONS: We found the performance of the BM test to be insufficiently accurate, as both over- and underdiagnosis of H. pylori infection were not infrequent. This test needs to be improved before its use in primary care can be recommended.

Adolescent↗
PubMed1998

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently.

BACKGROUND: Gastric mucosal surface hydrophobicity (GMSH) is an essential component of the mucosal defence system that is decreased by Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). Gastric ulcers occur predominantly in elderly subjects, and may thus reflect diminished mucosal resistance. AIMS: To investigate whether aging decreases GMSH. PATIENTS: One hundred and twenty patients without peptic ulcer disease were divided into three age groups: I (41 years or below); II (41-64 years); and III (65 years or above). METHODS: Biopsy specimens were taken from the antrum, corpus, and cardia for histology (Sydney system), urease testing for H pylori, and for contact angle measurement of GMSH with a goniometer. The presence of specific H pylori antibodies was checked by immunoblotting. RESULTS: Fifty two patients (43%) were infected, and 68 were uninfected with H pylori. GMSH at all biopsy sites was lower in H pylori infected subjects (p=0.0001), but also decreased with age independently of infection status (p=0.0001). The most notable decrease in GMSH occurred between age groups I and II in those with, and between age groups II and III in those without, H pylori infection. GMSH was greater in antral than in corpus mucosa in both infected (p=0.0001) and uninfected patients (p=0.0003). CONCLUSIONS: A physiological decrease in GMSH with aging may contribute to the risk of ulcer development in the elderly, and may act synergistically with H pylori and/or NSAIDs on gastric mucosal defence.

Adult↗
PubMed1997

Seroprevalence of Helicobacter pylori in German infants and children.

BACKGROUND: The purpose of the study was to evaluate the serological prevalence of Helicobacter pylori (H. pylori) infection during infancy and childhood in Germany. PATIENTS AND METHODS: We quantified specific IgG antibody titers against H. pylori by enzyme-linked immunosorbent assay (ELISA) technique (BIO-RAD G.A.P. IgG-test) from healthy children under 18 years (n = 216) admitted to hospital for minor surgical procedures. All patients were age 0-18 years and lived in the southern part of Germany (Bavaria and Baden-Wuerttemberg). For each age group, 12 different sera were obtained and were determined in duplicate. We analyzed the 216 sera within 6 age groups of equal size. Mean titers > 19 U/ml were considered positive for H. pylori infection. RESULTS: None of the sera of 48 children less than 4 years old were positive for anti-H. pylori specific IgG antibodies. Titers above 19 U/ml were found in 8.3% (3/36 sera each, CI 95% 1-21.7%) in the children age three to five and nine to 11 years. Six- to eight-year-old children showed a 19.4% seroprevalence (7/36 sera, CI 95% 8.2-48%) and children 12-14 years old showed a seropositivity of 16.7% (6/36 sera, CI 95% 6.6-46.1%). In contrast, 47.2% (17/36 sera, CI 26.5-70.3%) of the adolescents older than 14 years had positive H. pylori antibody titers (p < .01, compared to the age-group 12-14 years). The test for linear trend (seropositivity and age) was significant with p < .001. The overall incidence increase with age in prevalence of H. pylori infection was found to be 0.9% per year within this population. CONCLUSIONS: In contrast to published data from other European and non-European countries, we could not detect H. pylori infection in German infants less than four years old by measurement of IgG antibodies. In the older subjects, seropositivity increased significantly and linearly with age.

Adolescent↗
PubMed1996

Helicobacter pylori enzymes.

Helicobacter pylori exhibits a complex system of enzymes which serve a range of functions, such as colonization, damage of the host epithelium and provision of essential metabolic substrates. Colonization is favoured by urease and by the action on mucus and the mucosal barrier exerted by phospholipases and proteases, although this latter mechanism is controversial. Toxic effects are effected by urease, alcohol dehydrogenase (ADH), phospholipases and proteolytic enzymes. ADH produces acetaldehyde that is toxic to the mucosal cells, while phospholipases induce generation of products such as lysolecithin, which damage the gastric epithelium. Catalase and sodium dismutase of H. pylori are mainly involved in transforming toxic oxygen metabolites to harmless water; they protect the bacterium from the killing effect of neutrophils. Metabolic enzymes (for example, phosphatases, ATPases) are essential for the generation of energy, for synthesis and transport of cell products and for ion fluxes. In addition, they influence cell growth and the expression of virulence factors.

Acid Phosphatase↗
PubMed1996

Helicobacter pylori and proteolytic activity.

Protease activity of 10 different H. pylori strains, purified marker proteases and protease-positive reference bacteria (Klebsiella ozaenae, Serratia marcescens) were tested against bovine haemoglobin, porcine mucin, bovine serum albumin, gelatin and casein as substrates. After incubation in development buffer and subsequent staining with Coomassie blue, protease activity bands were demonstrated as transparent spots after polyacrylamide gel electrophoresis (PAGE) on gels with incorporated substrate. Presence of protease activity was investigated in a wide pH range (pH 2.0-9.0). Although marker proteases (0.15-0.2 microgram per slot) as well as protease-positive bacteria (2-30 micrograms per slot) clearly showed proteolytic activity in gels containing 0.1-0.2% protein mL-1, no proteolytic activity was demonstrated in any of the H. pylori strains tested. This finding indicates that H. pylori does not possess significant protease activity, as this would have been detected by this sensitive method.

Biopsy↗
PubMed1996

Prevalence of Helicobacter pylori infection and dyspepsia in young adults in Germany.

Data on the seroprevalence and time of acquisition of Helicobacter pylori (HP) infection in Germany are scarce. We studied the seroprevalence of HP infection and the relationship with gastrointestinal (Gl) symptoms in a group of 168 German medical students in the final year of their practical training and in 260 age-matched blood donors at the University of Ulm. Eight upper Gl symptoms were scored in a questionnaire, and blood samples were taken for the detection of HP lgG antibodies with an Enzyme Immunoassay (Bio-Rad). Values greater than 12.5 U/ml (positive) were detected in 50 medical students (28.8%) and in 96 blood donors (36.9%). At least one occasional Gl symptom was present in 71.4% of medical students and 70.7% of blood donors. When related to the HP status, 27.0% of HP negative and 32.9% of HP positive individuals were completely free of symptoms. Moderate to severe dyspeptic symptoms were reported by 17.4% of HP negative and 14.4% of HP positive individuals. We conclude that the seroprevalence of HP infection in young German adults is presently about 1/3 but that HP infection is not linked to gastrointestinal symptoms in this age class.

Adult↗
PubMed1994

Adhesion of Helicobacter pylori and Escherichia coli to human and bovine surface mucus cells in vitro.

Helicobacter pylori shows in vivo a specific affinity for epithelial surface mucus cells (SMC) of the human stomach. We studied the in vitro adhesion of five different H. pylori strains and one non-pathogenic Escherichia coli-strain to (a) human antral SMC, obtained during gastroscopy; (b) human tumour SMC, from a carcinoma cell line (CRL 1739 AGS); and (c) bovine SMC, obtained from the abomasum. SMC of different origin were characterized by means of electron microscopy and immunohistochemistry, and showed similar main features: all cells showed intra-cellular structures like zymogens and PAS-positive mucin granules. HSMC were antibody-positive against epithelial cell markers. All five H. pylori strains adhered to human SMC (HSMC) and tumour SMC (TSMC). Only one strain additionally adhered to bovine SMC (BSMC). No adhesion to any of these cells was observed with E. coli. Adhesion in vitro is characterized by a close membrane-to-membrane association between H. pylori and the target cells. This phenomenon suggests a specific receptor-ligand interaction.

Adenocarcinoma↗
PubMed1993

Ultrastructural localization of urease of Helicobacter pylori.

Helicobacter pylori urease was characterized by means of an enzyme histochemical electron microscopic technique. Ultrastructural analysis revealed no urease activity in one strain; in seven H. pylori strains (43.75%), urease activity was associated with the cell membrane. Eight strains (50.0%) showed reaction product located within the cytoplasm. Urease activity showed no correlation with localization of activity. Our results demonstrate that H. pylori urease is not uniform in all H. pylori strains, and differences in activity and localization of urease activity may account for different virulence activities.

Helicobacter pylori↗
PubMed1993

Coccoid like forms (CLF) of Helicobacter pylori. Enzyme activity and antigenicity.

In this study we attempted to transform "helical" forms of Helicobacter pylori to "coccoid like forms" (CLF) by induction with the following substances in vitro: bismuth subcitrate, bismuth subsalicylate, ampicillin, amoxicillin, erythromycin, ursodeoxycholic acid and glycochenodeoxycholic acid. Some liquid cultures were incubated for 24 days to induce CLF by aging. Changes in the protein pattern, urease enzyme activity and in the serological response against specific antigens were investigated. In all strains a significant but strain-variable rate of CLF was detected by induction of the tested substances. Beta-lactams and erythromycin generated a population of nearly 100% CLF, including many "spheroblasts". Relative induction rates by these substances were in the following order: beta-lactams and erythromycin > bismuth subcitrate > bismuth subsalicylate > bile acids. Strain variable reaction also was true for both inhibition of urease activity and influence on immunological response. Urease activity was lost in CLF induced by aging and was inhibited by bismuth salts. CLF induced by aging showed a loss of reactivity bands in the immunoblot. They always lost a 160 kD band and depending on the strain, 115 kD, 108 kD, 100 kD and 95 kD bands. Immunological response to the 120 kD band was reduced. Ultrastructural studies showed great degenerative changes of the cell wall in CLF induced by antibiotics but only few in CLF induced by bismuth salts and bile acids.

Anti-Bacterial Agents↗
PubMed1992

[Polymorphism in Helicobacter pylori--a key function in recurrence of infection?].

Despite the fact that Helicobacter (H.) pylori is ubiquitous throughout the world, little is known at present about the source of infection and mode of transmission. Person-to-person transmission may be of importance. The fact that Helicobacter pylori can revert to a coccoid form stimulated speculation about its role in transmission and as a possible cause of reinfection in duodenal ulcer disease. Various antibacterial agents (bismuth subcitrate 32 mg/l bismuth subsalicylate 64 mg/l, amoxicillin 0.05 mg/l, ampicillin 2 mg/l, erythromycin 4 mg/l, glycochenodeoxycholic acid 423 mg/l, ursodeoxycholic acid 540 mg/l) inhibit the growth of H. pylori and stimulate the formation of coccoid structures. Ultrastructural and biochemical results show that the coccoid form meets the necessary criteria for survival. Thus, to be successful, treatment must aim not only at eliminating the vegetative form, but also at preventing the development of the coccoid form.

Anti-Bacterial Agents↗
PubMed1991

In vitro inhibition of Helicobacter pylori urease: biochemical and ultrastructural analysis.

Inhibition of H. pylori urease was studied by means of electron-microscopy and electrophoretic methods using different urease inhibitors, such as acetohydroxamic-acid (AHA), L-ascorbic acid (AsA), copper ions, a combination of L-ascorbic acid with copper ions and UV light. AHA in two different concentrations and AsA at a concentration of 0.1 mg ml-1 showed incomplete inhibition of H. pylori urease activity in our electrophoretic experiments. Only membrane-bound activity was inhibited with AHA but not the activity localized within the cytoplasma as demonstrated by electron-microscopy. AsA at a concentration of 0.5 mg ml-1 and the combination of copper ions (1 microgram ml-1) with AsA completely inhibited the urease activity as demonstrated by electron-microscopy and electrophoretic experiments. Cu2+ ions in high concentrations (100 micrograms ml-1) and UV light exposure for more than 4 h induced a complete disintegration of H. pylori. Electrophoresis showed no active protein after UV light exposure of 2 h. Different urease inhibitors tested in this study showed dose-dependent inhibitory effects on H. pylori urease in vitro.

Ascorbic Acid↗