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논문 기본 정보

자료유형
학술저널
저자정보
Yuhua Chen (Division of Gastroenterology Union Hospital Tongji Medical College Huazhong University of Science a) Lei Zhang (Division of Gastroenterology Union Hospital Tongji Medical College Huazhong University of Science a) Yongbo Zhang (Department of Gastrointestinal Surgery Shandong Provincial Qianfoshan Hospital Shandong University) Tao Bai (Division of Gastroenterology Union Hospital Tongji Medical College Huazhong University of Science a) Jun Song (Division of Gastroenterology Union Hospital Tongji Medical College Huazhong University of Science a) Wei Qian (Division of Gastroenterology Union Hospital Tongji Medical College Huazhong University of Science a) Xiaohua Hou (Division of Gastroenterology Union Hospital Tongji Medical College Huazhong University of Science a)
저널정보
대한소화관운동학회(현 대한소화기능성질환.운동학회) Journal of Neurogastroenterology and Motility (JNM) Journal of Neurogastroenterology and Motility (JNM) Vol.26 No.3
발행연도
2020.1
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397 - 409 (13page)

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Background/AimsLipopolysaccharide (LPS) is the key factor inducing mucosal and systemic inflammation in various intestinal and parenteral diseases, which could initially disrupt the epithelial barrier function. EphrinA1/ephA2 is speculated to increase the epithelial permeability for its “repulsive interaction” between adjacent cells. This study aim to investigate the role of ephrinA1/ephA2 in LPS-induced epithelial hyperpermeability. MethodsIn vivo model challenged with oral LPS in C57BL/6 mice and in vitro model exposed to LPS in Caco2 monolayer were established. The barrier function was assessed including expression of tight junction proteins (occludin and claudin-1), transepithelial electrical resistance, and permeability to macromolecules (fluorescein isothiocyanate-labeled fluorescent dextran 4 kDa [FD4]). Moreover, the expression and phosphorylation of ephrinA1/ephA2 were quantified, and its roles in the process of epithelial barrier disruption were confirmed via stimulating ephA2 with ephrinA1-Fc chimera (ephrinA1-Fc) and inactivating ephA2 with ephA2-Fc chimera (ephA2-Fc), or ephA2 monoclonal antibody (ephA2-mab), as well as inhibiting extracellular signal-regulated kinase 1/2 (ERK1/2) with PD98059. ResultsLPS induced significant barrier dysfunction with dismissed occludin and claudin-1 expression, reduced transepithelial electrical resistance and increased FD4 permeability, accompanied by upregulated ephrinA1/ephA2 pathway and phosphorylation of ephA2 receptor. Furthermore, ephA2-Fc, and ephA2-mab ameliorated LPS-induced epithelial hyperpermeability, which was also inhibited by PD98059. Additionally, ephrinA1-Fc led to apparent epithelial leakage in Caco2 monolayer by promoting the phosphorylation of ERK1/2, which could be obviously blocked by ephA2-mab and PD98059. ConclusionEphrinA1/ephA2 promotes epithelial hyperpermeability with an ERK1/2-dependent pathway, which involves in LPS-induced intestinal barrier dysfunction.
#Lipopolysaccharides #Receptor #EphA2 #Receptor #Fc #Tight junction proteins

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참고문헌 (33)

참고문헌 신청
Rosadini CV / 2017 / Early innate immune responses to bacterial LPS / Curr Opin Immunol 44:14~19 google schola Hoogland IC / 2015 / Systemic inflammation and microglial activation : systematic review of animal experiments / J Neuroinflammation 12:114 google schola Cavaillon JM / 2018 / Exotoxins and endotoxins : inducers of inflammatory cytokines / Toxicon 149:45~53 google schola Vespasiani-Gentilucci U / 2018 / The role of intestinal microbiota in the pathogenesis of NAFLD : starting points for intervention / Arch Med Sci 14:701~706 google schola Chen X / 2017 / Blockade of high-mobility group box 1 attenuates intestinal mucosal barrier dysfunction in experimental acute pancreatitis / Sci Rep 7:6799 google schola

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