Apoptosis and upregulation of TNF-alpha and TRAIL receptor 1 (DR4) in the pathogenesis of food protein-induced enterocolitis syndrome.
10.3345/kjp.2010.53.4.525
- Author:
Jin Bok HWANG
1
;
Sang Pyo KIM
;
Yu Na KANG
;
Seong Ryong LEE
;
Seong Il SUH
;
Taeg Kyu KWON
Author Information
1. Department of Pediatrics, Keimyung University School of Medicine, Daegu, Korea. pedgi@kmu.ac.kr
- Publication Type:Original Article
- Keywords:
Food protein-induced enterocolitis syndrome;
Etiology;
Apoptosis;
Tumor necrosis factor-alpha;
TNF-related apoptosis-including ligand receptor 1
- MeSH:
Apoptosis;
Atrophy;
Cell Death;
Enterocolitis;
Epithelial Cells;
Fas Ligand Protein;
Humans;
Infant;
Intestine, Small;
Mucous Membrane;
Receptors, TNF-Related Apoptosis-Inducing Ligand;
Tumor Necrosis Factor-alpha;
Up-Regulation
- From:Korean Journal of Pediatrics
2010;53(4):525-531
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Expression levels of tumor necrosis factor (TNF)-alpha expression on the mucosa of the small intestine is increased in patients with villous atrophy in food protein-induced enterocolitis syndrome (FPIES). TNF-alpha 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-alpha, 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-alpha (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-alpha expression and DR4 pathway may have an important role in apoptosis.
