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우유 단백질 유발성 장염 증후군의 병리 기전으로 세포 자멸사와 TNF-α, TRAIL receptor 1 (DR4)의 발현 증가

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Author(s)
황진복김상표강유나이성룡서성일권택규
Keimyung Author(s)
Hwang, Jin BokKim, Sang PyoKang, Yu NaLee, Seong RyongSuh, Seong IlKwon, Taeg Kyu
Department
Dept. of Pediatrics (소아청소년학)
Dept. of Pathology (병리학)
Dept. of Pharmacology (약리학)
Dept. of Microbiology (미생물학)
Dept. of Immunology (면역학)
Institute for Medical Science (의과학연구소)
Journal Title
Korean Journal of Pediatrics
Issued Date
2010
Volume
53
Issue
4
Keyword
Food protein-induced enterocolitis syndromeEtiologyApoptosisTumor necrosis factor-alphaTNF-related apoptosis-including ligand receptor 1
Abstract
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.
목 적 : 융모 위축을 보이는 FPIES 환자의 소장 점막에는 TNF-α의 발현이 증가한다. TNF-α는 상피 세포의 세포 자렴사를 유발하는 것으로 알려져 있다. 저자들은 FPIES 병리생리의 특성을 알아 보고자 십이지장 점막 조직에서 TNF family와 TNF-수용체 family의 세포 자멸사를 연구하였다. 방 법 : 표준화된 경구 유발 시험을 통하여 FPIES로 진단된 15례의 환자와 5례의 대조군을 대상으로 연구하였다. 세포 자멸사를 확인하기 위하여 terminal deoxynucleotidyl transferase-me-diated dUTP nick end-labeling (TUNEL) 염색을 시행하였다. 세포 자멸의 기전을 알아 보기 위해 TNF family의 TNF-α, Fas ligand (FasL)와 TNF-수용체 family의 TNF-related apoptosis-including ligand (TRAIL) receptor 1 (DR4), TRAIL receptor 2 (DR5), Fas를 면역조직화학으로 염색하였다. 결 과 : TUNEL+ 세포는 대조군에 비하여 FPIES 환자군의 십이지장 점막에서 의미 있게 높게 발현하였다(P =0.043). TNF- α (P=0.0001)와 DR4 (P =0.003)도 대조군에 비하여 FPIES군에서 의미 있게 높게 발현하였다. FasL, Fas, DR5의 발현은 두 군 모두에서 낮았으며, 두 군간에 의미 있는 차이를 보이지도 않았다. 결 론 : FPIES의 병리생리는 세포 자멸사에 의하여 발생하며, TNF-α의 발현과 DR4 경로가 세포 자멸사에서 중요한 역할을 하는 것으로 추정된다.
Alternative Title
Apoptosis and upregulation of TNF-α and TRAIL receptor 1 (DR4) in the pathogenesis of food protein-induced enterocolitis syndrome
Keimyung Author(s)(Kor)
황진복
김상표
강유나
이성용
서성일
권택규
Publisher
School of Medicine
Citation
황진복 et al. (2010). 우유 단백질 유발성 장염 증후군의 병리 기전으로 세포 자멸사와 TNF-α, TRAIL receptor 1 (DR4)의 발현 증가. Korean Journal of Pediatrics, 53(4), 525–531. doi: 10.3345/kjp.2010.53.4.525
Type
Article
ISSN
1738-1061
DOI
10.3345/kjp.2010.53.4.525
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/36224
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
1. School of Medicine (의과대학) > Dept. of Microbiology (미생물학)
1. School of Medicine (의과대학) > Dept. of Pathology (병리학)
1. School of Medicine (의과대학) > Dept. of Pediatrics (소아청소년학)
1. School of Medicine (의과대학) > Dept. of Pharmacology (약리학)
3. Research Institutues (연구소) > Institute for Medical Science (의과학연구소)
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