CYTOSKELETAL DISARRANGEMENT IN RAT INTESTINAL EPITHELIUM AFTER IN VIVO EXPOSURE TO SECRETAGOGUES
Identifieur interne : 003611 ( Main/Exploration ); précédent : 003610; suivant : 003612CYTOSKELETAL DISARRANGEMENT IN RAT INTESTINAL EPITHELIUM AFTER IN VIVO EXPOSURE TO SECRETAGOGUES
Auteurs : H. Hansson [Suède] ; Stefan Lange [Suède] ; Ivar Lönnroth [Suède] ; Björn Rozell [Suède] ; Harold Tinberg [États-Unis]Source :
- Acta Pathologica Microbiologica Scandinavica Series B: Microbiology [ 0108-0180 ] ; 1984-09.
English descriptors
- Teeft :
- Acta path, Actin, Actin filaments, Adenylate, Adenylate cyclase, Apical, Apical part, Bovine serum albumin, Cell biol, Central core, Chloroquine, Chlorpromazine, Cholera, Cholera toxin, Cholera toxoid, Colchicine, Coli, Cyclase, Cytochalasin, Cytoskeletal, Cytoskeletal components, Cytoskeleton, Disorganization, Electron micrograph, Enterotoxin, Epithelial, Epithelial cells, Epithelium, Filament, Fluid accumulation, Fluid hypersecretion, Fluid secretion, Hypersecretion, Immunofluorescence microscopy, Intermediate filaments, Intestinal, Intestinal epithelial cells, Intestinal epithelium, Keratin, Keratin filaments, Microfilaments, Microvilli, Microvilli region, Small intestine, Toxin, Villus.
Abstract
Cholera toxin (CT) and E. coli heat‐labile enterotoxin (LT) induced hypersecretion in the small intestine, as did cytochalasin B and dibutyryl‐cyclic AMP (DB‐cAMP). The cytoskeleton in the apical part of the intestinal epithelial cells was disorganized after challenge with either of the four secretagogues, but not cholera B‐subunit toxoid, as revealed by immunofluorescence microscopy using actin and the intermediate filament keratin as markers. Electron microsocopic analysis confirmed the re‐engagement of the terminal web and the appearance of short microvilli lacking most of their normally observed central core of actin filaments. Pretreatment with chloroquine prevented cytoskeletal disorganization as well as hypersecretion by CT. but not by cytochalasin B. A similar effect was achieved with chloroquine on CT‐induced fluid secretion, while chlorpromazine inhibited the fluid response to cytochalasin B as well as to CT. The observed cytoskeletal re‐engagement might be one of the reactions behind enterotoxic diarrhoea.
Url:
DOI: 10.1111/j.1699-0463.1984.tb02801.x
Affiliations:
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Pettis Memorial V. A. Hospital</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Acta Pathologica Microbiologica Scandinavica Series B: Microbiology</title><title level="j" type="alt">ACTA PATHOLOGICA MICROBIOLOGICA SCANDINAVICA SERIES B MICROBIOLOGY</title><idno type="ISSN">0108-0180</idno><idno type="eISSN">1600-0463</idno><imprint><biblScope unit="vol">92B</biblScope><biblScope unit="issue">1‐6</biblScope><biblScope unit="page" from="93">93</biblScope><biblScope unit="page" to="99">99</biblScope><biblScope unit="page-count">7</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1984-09">1984-09</date></imprint><idno type="ISSN">0108-0180</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0108-0180</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acta path</term><term>Actin</term><term>Actin filaments</term><term>Adenylate</term><term>Adenylate cyclase</term><term>Apical</term><term>Apical part</term><term>Bovine serum albumin</term><term>Cell biol</term><term>Central core</term><term>Chloroquine</term><term>Chlorpromazine</term><term>Cholera</term><term>Cholera toxin</term><term>Cholera toxoid</term><term>Colchicine</term><term>Coli</term><term>Cyclase</term><term>Cytochalasin</term><term>Cytoskeletal</term><term>Cytoskeletal components</term><term>Cytoskeleton</term><term>Disorganization</term><term>Electron micrograph</term><term>Enterotoxin</term><term>Epithelial</term><term>Epithelial cells</term><term>Epithelium</term><term>Filament</term><term>Fluid accumulation</term><term>Fluid hypersecretion</term><term>Fluid secretion</term><term>Hypersecretion</term><term>Immunofluorescence microscopy</term><term>Intermediate filaments</term><term>Intestinal</term><term>Intestinal epithelial cells</term><term>Intestinal epithelium</term><term>Keratin</term><term>Keratin filaments</term><term>Microfilaments</term><term>Microvilli</term><term>Microvilli region</term><term>Small intestine</term><term>Toxin</term><term>Villus</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cholera toxin (CT) and E. coli heat‐labile enterotoxin (LT) induced hypersecretion in the small intestine, as did cytochalasin B and dibutyryl‐cyclic AMP (DB‐cAMP). The cytoskeleton in the apical part of the intestinal epithelial cells was disorganized after challenge with either of the four secretagogues, but not cholera B‐subunit toxoid, as revealed by immunofluorescence microscopy using actin and the intermediate filament keratin as markers. Electron microsocopic analysis confirmed the re‐engagement of the terminal web and the appearance of short microvilli lacking most of their normally observed central core of actin filaments. Pretreatment with chloroquine prevented cytoskeletal disorganization as well as hypersecretion by CT. but not by cytochalasin B. A similar effect was achieved with chloroquine on CT‐induced fluid secretion, while chlorpromazine inhibited the fluid response to cytochalasin B as well as to CT. The observed cytoskeletal re‐engagement might be one of the reactions behind enterotoxic diarrhoea.</div></front></TEI><affiliations><list><country><li>Suède</li><li>États-Unis</li></country></list><tree><country name="Suède"><noRegion><name sortKey="Hansson, H" sort="Hansson, H" uniqKey="Hansson H" first="H." last="Hansson">H. Hansson</name></noRegion><name sortKey="Hansson, H" sort="Hansson, H" uniqKey="Hansson H" first="H." last="Hansson">H. Hansson</name><name sortKey="Lange, Stefan" sort="Lange, Stefan" uniqKey="Lange S" first="Stefan" last="Lange">Stefan Lange</name><name sortKey="Lonnroth, Ivar" sort="Lonnroth, Ivar" uniqKey="Lonnroth I" first="Ivar" last="Lönnroth">Ivar Lönnroth</name><name sortKey="Rozell, Bjorn" sort="Rozell, Bjorn" uniqKey="Rozell B" first="Björn" last="Rozell">Björn Rozell</name></country><country name="États-Unis"><noRegion><name sortKey="Tinberg, Harold" sort="Tinberg, Harold" uniqKey="Tinberg H" first="Harold" last="Tinberg">Harold Tinberg</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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