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CYTOSKELETAL DISARRANGEMENT IN RAT INTESTINAL EPITHELIUM AFTER IN VIVO EXPOSURE TO SECRETAGOGUES
Author(s) -
HANSSON H.A.,
LANGE STEFAN,
LöNNROTH IVAR,
ROZELL BJöRN,
TINBERG HAROLD
Publication year - 1984
Publication title -
acta pathologica microbiologica scandinavica series b: microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0108-0180
DOI - 10.1111/j.1699-0463.1984.tb02801.x
Subject(s) - cytoskeleton , cholera toxin , cytochalasin , cytochalasin b , microbiology and biotechnology , actin , biology , microfilament , cytochalasin d , secretion , epithelium , microtubule , chemistry , in vitro , endocrinology , biochemistry , cell , genetics
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.