Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0740441 (acute diarrhea)
 2,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Citrinin fed to mature laying hens at levels of 0, 50, and 250 mug/g. of diet for three weeks had no effect on body weight, feed consumption, egg production, egg weight or egg shell quality. A moderate diarrhea occurring about three days after feeding 250 mug. citrinin/g. of diet was observed. However, the diarrhea subsided once the birds were returned to a normal diet. Young broiler chicks were fed a diet containing either 0, 62.5, 125, 250, or 500 mug. citrinin/g. of diet from hatching to three weeks of age. Body weight was decreased by the 500 mug/g. level whereas all levels of citrinin resulted in enlarged kidneys and an improvement in feed conversion when compared to control values. There was also a slight dose-related increase in liver size. The 250 and 500 mug./g. levels resulted in a dose-related increase in water consumption accompanied by an acute diarrhea. Dietary citrinin had no effect on serum protein, glucose, cholesterol, uric acid, calcium, potassium and sodium concentrations or packed cell volume.
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PMID:Effect of citrinin, a mycotoxin produced by Penicillium citrinum, on laying hens and young broiler chicks. 95 61

Disruption of the intestinal epithelial barrier occurs in many intestinal diseases, but neither the mechanisms nor the contribution of barrier dysfunction to disease pathogenesis have been defined. We utilized a murine model of T cell-mediated acute diarrhea to investigate the role of the epithelial barrier in diarrheal disease. We show that epithelial barrier dysfunction is required for the development of diarrhea. This diarrhea is characterized by reversal of net water flux, from absorption to secretion; increased leak of serum protein into the intestinal lumen; and altered tight junction structure. Phosphorylation of epithelial myosin II regulatory light chain (MLC), which has been correlated with tight junction regulation in vitro, increased abruptly after T cell activation and coincided with the development of diarrhea. Genetic knockout of long myosin light chain kinase (MLCK) or treatment of wild-type mice with a highly specific peptide MLCK inhibitor prevented epithelial MLC phosphorylation, tight junction disruption, protein leak, and diarrhea following T cell activation. These data show that epithelial MLCK is essential for intestinal barrier dysfunction and that this barrier dysfunction is critical to pathogenesis of diarrheal disease. The data also indicate that inhibition of epithelial MLCK may be an effective non-immunosuppressive therapy for treatment of immune-mediated intestinal disease.
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PMID:Epithelial myosin light chain kinase-dependent barrier dysfunction mediates T cell activation-induced diarrhea in vivo. 1618 95