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Biomedical subjects

S Lange

Publications and source records attributed to S Lange.

At least 181 records · Page 10Linked to original sources
PubMed1984

Studies on cholera-toxin-induced desensitization of adenylate cyclase in the mouse intestinal mucosa.

Repeated peroral pretreatment ('immunization') with cholera toxin (CT) in mice induces protection against CT as well as against prostaglandin E1 (PGE1), as evaluated by fluid accumulation in intestinal loops. The fluid response to CT is depressed for more than 1 month, while the response to PGE1 is inhibited for 4-7 days after the pretreatment. Immunofluorescence microscopy revealed that neither the binding nor the penetration of CT into the intestinal epithelial cells is affected by the toxin pretreatment. Furthermore, the CT-induced release of mucus in goblet cells is not influenced by the toxin pretreatment. In contrast, the enzyme adenylate cyclase (AC), which mediates the actions of CT and PGE1, shows a long-lasting desensitization to CT, as estimated in mucosal membrane preparations. Chlorpromazine and cycloheximide revert the desensitization to CT as well as to PGE1. The present data suggest that intestinal resistance to CT in the mouse is due to desensitization of the reaction between CT and AC and requires stimulation of AC, as well as an active protein synthesis.

Adenylyl Cyclases↗
PubMed1984

Development of mucous cells in mouse intrapulmonary airways induced by cholera toxin, dibutyryl cyclic AMP and prostaglandin E1.

The effect of cholera toxin (CT), dibutyryl cyclic adenosinemonophosphate (DE-cAMP) and prostaglandin E1 (PGE1) on the morphological appearance of mouse intrapulmonary airway epithelium has been studied. All three secretagogues, known to mediate their activity via cAMP, induced increased numbers of mucous cells, but with different kinetics. After exposure to DB-cAMP, mucous cells appeared after 7 h with a peak value at 48 h. The corresponding values for PGE1 were 24 h for the appearance and 48 h for peak value whereas exposure to CT gave a lower response with a peak at 72 h. Autoradiography of lungs from mice injected with 3H-thymidine showed that the mucous cells appeared without any foregoing DNA synthesis, however, increased numbers of labelled cells were seen as a late response to the secretagogues.

Adenylyl Cyclases↗
PubMed1984

Inhibition of cyclic AMP-mediated intestinal hypersecretion by pituitary extracts from rats pretreated with cholera toxin.

Peroral pretreatment with cholera toxin (CT) in rats induced protection against intestinal hypersecretion by CT or prostaglandin E1 (PGE1). Pituitary glands from these CT-pretreated rats were homogenized and injected intravenously or intraluminally into untreated rats. These recipients became resistant to CT- as well as to PGE1-induced hypersecretion; recipients given pituitary extracts from control animals responded normally. Extracts of intestinal mucosa from CT-pretreated, but not from control rats, also inhibited secretion by CT. Ultrafiltration experiments with the pituitary or intestinal extracts indicated that the antisecretory factors had a molecular weight between 10,000 and 50,000.

Alprostadil↗
PubMed1984

Protection against experimental cholera in the rat. A study on the formation of antibodies against cholera toxin and desensitization of adenylate cyclase after immunization with cholera toxin.

The importance of antibodies to cholera toxin (CT) versus desensitization of intestinal adenylate cyclase for protection against experimental cholera in the rat was investigated. Animals were immunized five times with CT either perorally or intravenously; antitoxic antibodies were measured in both serum and bile, and intestinal anti-CT-containing plasma cells (ACC) as well as eosinophilic leucocytes were counted. Both peroral and intravenous immunizations induced high levels of serum antibodies, while antibodies in bile appeared only after peroral immunization. The number of eosinophilic leucocytes in the intestinal mucosa increased in response to peroral immunization. CT-induced stimulation of intestinal adenylate cyclase was significantly suppressed, i.e., desensitized, after peroral immunization, but was equally stimulated in intravenous immunized and in control animals. A constant and long-lasting protection against CT-induced secretion was obtained after peroral immunization. This protection correlated neither to the concentrations of antitoxic antibodies in serum, nor to those in bile, nor to the number of ACC, but did correlate to the desensitization of adenylate cyclase.

Adenylyl Cyclases↗
PubMed1983

Influence of bile acids on cholera toxin-induced secretion in mouse jejunum.

The influence of bile acids on intestinal secretion induced by cholera toxin (CT) was studied in mice. The secretion was examined in ligated loops after the bile flow had been stopped by ligation of the common bile duct (CD). Bile depletion was found to inhibit both the secretion induced by CT, the degradation of CT, and the binding of CT to epithelial cells--all of which could be restored to normal by the application, before CT challenge, of bile acids in the loops of CD-ligated mice. Out of the nine bile acids tested, cholic acid, deoxycholic acid and chenodeoxycholic acid were the most potent, their ED50 values being 0.2, 0.2, and 0.6 mM respectively.

Animals↗
PubMed1983

Toxin A of Clostridium difficile: production, purification and effect in mouse intestine.

Clostridium difficile produces one diarrhoeogenic toxin designed A, and one cytopathogenic toxin designed B. Toxin A was purified in a four-step-fractionation procedure. In the last purification step the toxin was separated by elution with galactose from an agarose gel. The purified toxin A induced a clear and watery hypersecretion in intestinal loops of mouse, while mixtures of toxin A and B induced a haemorrhagic secretion. At an ED50 value for the purified toxin A of 0.5 microgram there was a brief, optimal hypersecretion after four hours. Like the fluid secretion induced by cholera toxin, that induced by toxin A could be inhibited by chlorpromazine or by depletion of intestinal bile. In contrast to cholera toxin, however, toxin A did not activate intestinal adenylate cyclase--at least not permanently. Antisera which neutralized cholera toxin did not neutralize toxin A, and vice versa.

Adenylyl Cyclases↗
PubMed1982

[The effect of beta-receptor blockers and cardiac glycosides on the heart rate, systolic blood pressure and ST interval in submaximal ergometer exertion].

14 males at the age of 49 +/- 6.4 years with condition after myocardial infarction were loaded on the bicycle ergometer according to the criteria of the WHO. After injection of a beta-receptor blocker at the submaximal functional level the product of the pressure frequency decreased by 25% and the watt-pulse increased by 17%. The oxygen pulse and the respiratory quotient remained constant. An additional injection of glycosides did not significantly change these parameters. At the same time no falsely positive evidence concerning the behaviour of the ST-distance as criterium of withdrawal was provoked. The results of the submaximal and symptom-limited function were not falsified in the therapy with beta-receptor-blockers and glycosides, when the criteria of withdrawal recommended by the WHO are used unchangedly.

Adult↗
PubMed1982

Establishment and characterization of chicken embryo fibroblast clone LSCC-H32.

Cell line CEC-32 and clone LSCC-H32 were established from primary chicken embryo cells spontaneously but not experimentally transformed at 32 degrees C. The lines consisted of fibroblastoid and polygonal cells and had a subtetraploid karyotype of 2N = 130 to 140. The cells showed increased plating efficiency and metabolic activities as demonstrated by hexose uptake and plasminogen activator assay. The established cells produced avian lymphoid leukosis viruses of subgroups A and B. The virus released from LSCC-H32 cells induced lymphoid leukosis in inoculated chickens 18 to 22 wk post infection (PI). The cells have been carried in continuous culture for 285 passages and they appeared to grow indefinitely. They were efficiently used to propagate several animal viruses and to titrate chicken interferon.

Alpharetrovirus↗
PubMed1982

Potentiating effect of bile on enterotoxin-induced diarrhea.

The influence of bile acids on adenosine 3',5'-phosphate-induced intestinal secretion was studied in mice. Bile flow was stopped by ligation of the common bile duct, and secretion was induced in ligated loops of the small intestine. The decrease of bile led to inhibition of hypersecretion after challenge with heat-labile enterotoxins from Vibrio cholerae and Escherichia coli, as well as with prostaglandin E1. In contrast, the fluid response induced by dibutyryl-adenosine 3',5'-phosphate was unaffected by intestinal bile. Injection of bile or bile acids into intestinal loops before cholera toxin challenge restored the toxin-induced secretion in the bile-depleted intestine. At the subcellular level the decrease of intestinal bile led to inhibition of cholera toxin-activated adenylate cyclase, whereas the bile concentration did not influence the binding of 125I-labeled toxin to the intestinal epithelial cells. The results suggest that intestinal bile interacts with adenylate cyclase in the induction of fluid secretion by enterotoxins and prostaglandin E1.

Adenylyl Cyclases↗
PubMed1981

Diffusion-in-gel enzyme linked immunosorbent assay (DIG-ELISA) for detection of antibodies to Yersinia enterocolitica O:3.

The Diffusion-In-Gel Enzyme Linked Immunosorbent Assay (DIG-ELISA) is a new and simple method for the quantitation of antibodies to diffuse from wells in gel in petri dishes and absorb to an antigen coated to the plastic surface prior to testing. The antigen-antibody reaction is visualized with horseradish-peroxidase conjugated class-specific anti-immunoglobulins. The DIG-ELISA permits detection of 0.1 microns/ml of specific antibodies. This method was used to determine the IgG, IgA and IgM antibody levels to Yersinia enterocolitica O:3 in sera from patients with antibody titres to this microorganism, as determined by direct agglutination and complement-fixation test. The DIG-ELISA IgG antibody values, in contrast to IgA and IgM, correlated well to titres obtained by the direct agglutination method. Low degrees of correlations were found for all three immunoglobulin classes when compared to the complement fixation test.

Antibodies, Bacterial↗
PubMed1981

A new principle for resistance to cholera: desensitization to cyclic AMP-mediated diarrhea induced by cholera toxin in the mouse intestine.

The mechanisms behind the intestinal resistance to cholera toxin was studied in a mouse model. Repeated peroral treatments with cholera toxin (CT) led to a long-lasting inhibition of the toxin-induced activation of intestinal adenylate cyclase (AC). A corresponding inhibition of the intestinal fluid secretion induced not only by CT but also by prostaglandin E1 was observed. This unspecific desensitization was followed by a CT-specific inhibition of secretion and AC after 8 to 16 days. The desensitization to CT was totally reversed by a 4 hour-treatment with cycloheximide, an inhibitor of protein synthesis. Neither the secretory response to dibutyryl-cyclic AMP nor the activity of soluble phosphodiesterase differed between the CT-treated mice and the control group. Nor was the average turn-over rate of intestinal cells changed as judged from the mucosal incorporation of [3H]-thymidine. It is postulated that intestinal resistance to CT is mainly a function of AC-desensitization mediated by an inducible protein.

3',5'-Cyclic-AMP Phosphodiesterases↗