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KMID : 1130320100530040525
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Korean Journal of Pediatrics
2010 Volume.53 No. 4 p.525 ~ p.531
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Apoptosis and upregulation of TNF-α and TRAIL receptor 1 (DR4) in the pathogenesis of food protein-induced enterocolitis syndrome
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Hwang Jin-Bok
Kim Sang-Pyo
Kang Yu-Na
Lee Seong-Ryong
Suh Seong-Il
Kwon Taeg-Kyu
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Abstract
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Purpose: Expression levels of tumor necrosis factor (TNF)-α expression on the mucosa of the small intestine is increased in patients with villous atrophy in food protein-induced enterocolitis syndrome (FPIES). TNF-α has been reported to induce apoptotic cell death in the epithelial cells. We studied the TNF family and TNF-receptor family apoptosis on the duodenal mucosa to investigate their roles in the pathogenesis of FPIES.
Methods: Fifteen infants diagnosed as having FPIES using standard oral challenge test and 5 controls were included. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining was performed to identify the apoptotic cell death bodies. Immunohistochemical staining of TNF-α, Fas ligand (FasL) for TNF family and TNF-related apoptosis-including ligand (TRAIL) receptor 1 (DR4), TRAIL receptor 2 (DR5), and Fas for TNF-receptor family were performed to determine the apoptotic mechanisms.
Results: TUNEL+ was significantly more highly expressed in the duodenal mucosa of FPIES patients than in controls (P = 0.043). TNF-α (P =0.0001) and DR4 (P =0.003) were significantly more highly expressed in FPIES patients than in controls. Expression levels of FasL, Fas, and DR5 were low in both groups and were not significantly different between the 2 groups.
Conclusion: These results suggest that FPIES pathogenesis is induced by apoptosis, and that TNF-α expression and DR4 pathway may have an important role in apoptosis.
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KEYWORD
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Food protein-induced enterocolitis syndrome, Etiology, Apoptosis, Tumor necrosis factor-alpha, TNF-related apoptosis-including ligand receptor 1
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