Apoptosis and upregulation of TNF-alpha and TRAIL receptor 1 (DR4) in the pathogenesis of food protein-induced enterocolitis syndrome / 소아과
Korean Journal of Pediatrics
;
: 525-531, 2010.
Article
in Korean
| WPRIM
| ID: wpr-43756
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Atrophy
/
Up-Regulation
/
Tumor Necrosis Factor-alpha
/
Cell Death
/
Apoptosis
/
Enterocolitis
/
Epithelial Cells
/
Fas Ligand Protein
/
Receptors, TNF-Related Apoptosis-Inducing Ligand
/
Intestine, Small
Type of study:
Etiology study
/
Prognostic study
Limits:
Humans
/
Infant
Language:
Korean
Journal:
Korean Journal of Pediatrics
Year:
2010
Type:
Article
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