Journal of Molecular Histology

, Volume 45, Issue 2, pp 217–227

Disturbance of intraepithelial lymphocytes in a murine model of acute intestinal ischemia/reperfusion

Authors

  • Yuan Qiu
    • Department of General Surgery, Xinqiao HospitalThird Military Medical University
  • Min Yu
    • Department of General Surgery, Xinqiao HospitalThird Military Medical University
  • Yang Yang
    • Department of General Surgery, Xinqiao HospitalThird Military Medical University
  • Halei Sheng
    • Center of Medical Experiment and Technology, Xinqiao HospitalThird Military Medical University
  • Wensheng Wang
    • Department of General Surgery, Xinqiao HospitalThird Military Medical University
  • Lihua Sun
    • Department of General Surgery, Xinqiao HospitalThird Military Medical University
  • Guoqing Chen
    • Department of General Surgery, Xinqiao HospitalThird Military Medical University
  • Yong Liu
    • Department of General Surgery, Xinqiao HospitalThird Military Medical University
  • Weidong Xiao
    • Department of General Surgery, Xinqiao HospitalThird Military Medical University
    • Department of General Surgery, Xinqiao HospitalThird Military Medical University
Original Paper

DOI: 10.1007/s10735-013-9544-1

Cite this article as:
Qiu, Y., Yu, M., Yang, Y. et al. J Mol Hist (2014) 45: 217. doi:10.1007/s10735-013-9544-1

Abstract

Strategically located at the epithelial basolateral surface, intraepithelial lymphocytes (IELs) are intimately associated with epithelial cells and maintain the epithelial barrier integrity. Intestinal ischemia–reperfusion (I/R)-induced acute injury not only damages the epithelium but also affects the mucosal barrier function. Therefore, we hypothesized that I/R-induced mucosal damage would affect IEL phenotype and function. Adult C57BL/6J mice were treated with intestinal I/R or sham. Mice were euthanized at 6 h after I/R, and the small bowel was harvested for histological examination and to calculate the transmembrane resistance. Occludin expression and IEL location were detected through immunohistochemistry. The IEL phenotype, activation, and apoptosis were examined using flow cytometry. Cytokine and anti-apoptosis-associated gene expressions were measured through RT-PCR. Intestinal I/R induced the destruction of epithelial cells and intercellular molecules (occludin), resulting in IEL detachment from the epithelium. I/R also significantly increased the CD8αβ, CD4, and TCRαβ IEL subpopulations and significantly changed IEL-derived cytokine expression. Furthermore, I/R enhanced activation and promoted apoptosis in IELs. I/R-induced acute intestinal mucosal damage significantly affected IEL phenotype and function. These findings provide profound insight into potential IEL-mediated epithelial barrier dysfunction after intestinal I/R.

Keywords

Ischemia–reperfusion Injury Intestinal epithelium Intraepithelial lymphocytes

Copyright information

© Springer Science+Business Media Dordrecht 2013