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Expression of transforming growth factor β1, transforming growth factor type I and II receptors, and TNF-α in the mucosa of the small intestine in infants with food protein–induced enterocolitis syndrome

Background: TNF-α secreted by activated T cells is known to increase intestinal permeability, whereas transforming growth factor (TGF) β has the ability to protect the epithelial barrier. Objective: We determined the expression of TGF-β1, its receptors, and TNF-α on the mucosa of small intestine to...

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Published in:Journal of allergy and clinical immunology 2002-01, Vol.109 (1), p.150-154
Main Authors: Chung, Hai Lee, Hwang, Jin Bok, Park, Jeong Ja, Kim, Sang Gyung
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description Background: TNF-α secreted by activated T cells is known to increase intestinal permeability, whereas transforming growth factor (TGF) β has the ability to protect the epithelial barrier. Objective: We determined the expression of TGF-β1, its receptors, and TNF-α on the mucosa of small intestine to investigate their roles in the pathogenesis of food protein–induced enterocolitis syndrome (FPIES). Methods: Twenty-eight infants diagnosed with FPIES by means of clinical criteria and challenge test results were included. Immunohistochemical stains for TGF-β1, type 1 and 2 TGF-β receptors, and TNF-α on duodenal biopsy specimens were performed. Results: TGF-β1 expression was generally depressed in patients. Expression of type 1 TGF-β receptor was significantly lower in the patients who had villous atrophy compared with expression in those patients who did not (P < .001) and negatively correlated with the severity of atrophy (r = –0.59, P < .001). Expression of type 2 TGF-β receptor showed no significant difference between the patients with or without villous atrophy. The immunoreactivity for both TGF-β receptors on lamina proprial cells was slight or negative. TNF-α expression was detected on both epithelial and lamina proprial cells and was significantly greater in the patients who had villous atrophy compared with that in the patients who did not (P < .01). Conclusion: Our results suggest that decreased countering activity of TGF-β1 against T-cell cytokines is implicated in the pathogenesis of FPIES. The significantly lower expression of type 1 TGF-β receptor compared with type 2 receptor suggests the differential contribution of each receptor to the diverse biologic activities of TGF-β in the intestinal epithelium. (J Allergy Clin Immunol 2002;109:150-4.)
doi_str_mv 10.1067/mai.2002.120562
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Objective: We determined the expression of TGF-β1, its receptors, and TNF-α on the mucosa of small intestine to investigate their roles in the pathogenesis of food protein–induced enterocolitis syndrome (FPIES). Methods: Twenty-eight infants diagnosed with FPIES by means of clinical criteria and challenge test results were included. Immunohistochemical stains for TGF-β1, type 1 and 2 TGF-β receptors, and TNF-α on duodenal biopsy specimens were performed. Results: TGF-β1 expression was generally depressed in patients. Expression of type 1 TGF-β receptor was significantly lower in the patients who had villous atrophy compared with expression in those patients who did not (P &lt; .001) and negatively correlated with the severity of atrophy (r = –0.59, P &lt; .001). Expression of type 2 TGF-β receptor showed no significant difference between the patients with or without villous atrophy. The immunoreactivity for both TGF-β receptors on lamina proprial cells was slight or negative. TNF-α expression was detected on both epithelial and lamina proprial cells and was significantly greater in the patients who had villous atrophy compared with that in the patients who did not (P &lt; .01). Conclusion: Our results suggest that decreased countering activity of TGF-β1 against T-cell cytokines is implicated in the pathogenesis of FPIES. The significantly lower expression of type 1 TGF-β receptor compared with type 2 receptor suggests the differential contribution of each receptor to the diverse biologic activities of TGF-β in the intestinal epithelium. 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Objective: We determined the expression of TGF-β1, its receptors, and TNF-α on the mucosa of small intestine to investigate their roles in the pathogenesis of food protein–induced enterocolitis syndrome (FPIES). Methods: Twenty-eight infants diagnosed with FPIES by means of clinical criteria and challenge test results were included. Immunohistochemical stains for TGF-β1, type 1 and 2 TGF-β receptors, and TNF-α on duodenal biopsy specimens were performed. Results: TGF-β1 expression was generally depressed in patients. Expression of type 1 TGF-β receptor was significantly lower in the patients who had villous atrophy compared with expression in those patients who did not (P &lt; .001) and negatively correlated with the severity of atrophy (r = –0.59, P &lt; .001). Expression of type 2 TGF-β receptor showed no significant difference between the patients with or without villous atrophy. The immunoreactivity for both TGF-β receptors on lamina proprial cells was slight or negative. TNF-α expression was detected on both epithelial and lamina proprial cells and was significantly greater in the patients who had villous atrophy compared with that in the patients who did not (P &lt; .01). Conclusion: Our results suggest that decreased countering activity of TGF-β1 against T-cell cytokines is implicated in the pathogenesis of FPIES. The significantly lower expression of type 1 TGF-β receptor compared with type 2 receptor suggests the differential contribution of each receptor to the diverse biologic activities of TGF-β in the intestinal epithelium. 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subjects Allergic diseases
Biological and medical sciences
Digestive allergic diseases
Food protein–induced enterocolitis syndrome
Immunopathology
Medical sciences
TNFα
transforming growth factor β
transforming growth factor β receptors
title Expression of transforming growth factor β1, transforming growth factor type I and II receptors, and TNF-α in the mucosa of the small intestine in infants with food protein–induced enterocolitis syndrome
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