Exogenous carcinoembryonic antigen-related cell adhesion molecule 1 suppresses 2,4,6-trinitrobenzene sulfonic acid-induced ulcerative colitis in mice

J Surg Res. 2015 May 1;195(1):113-20. doi: 10.1016/j.jss.2015.01.025. Epub 2015 Jan 21.

Abstract

Background: Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is known to play an immunomodulatory role in a variety of tumors, but its role in ulcerative colitis (UC) remains to be elucidated. The present study aimed to investigate the effects of exogenous CEACAM1 on UC using a mouse model.

Materials and methods: UC in female Balb/c mice was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS). Hundred microliters of 1% TNBS was supplied through abdominal smearing for sensitization. Then after 7 d, 100 μL 0.5% TNBS was administered by a transrectal injection. After injection, the mice were placed in an upside-down position for 1 min. The CEACAM1 treatment was performed by receiving a transrectal injection of 10(9) pfu of CEACAM1. The mice were weighed, and the colonic mucosa damage was scored. The effects of exogenous CEACAM1 expression on mouse colon inflammation, apoptosis, and CD4 T lymphocyte infiltration in UC were examined.

Results: CEACAM1 expression was significantly reduced in the colon tissue of mice with UC, and the expression of exogenous CEACAM1 improved the symptoms of UC, as evidenced by hematoxylin-eosin staining and histopathologic scores. Moreover, exogenous CEACAM1 reduced the levels of inflammatory cytokines, suppressed CD4 T cell infiltration, and effectively inhibited apoptosis in the colon of TNBS-induced UC mice.

Conclusions: The expression of exogenous CEACAM1 effectively rescues the symptoms of TNBS-induced UC in mice by inhibiting inflammation, T cell infiltration, and apoptosis in the colon.

Keywords: Apoptosis; CEACAM1; Inflammation; Ulcerative colitis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Carcinoembryonic Antigen / genetics
  • Carcinoembryonic Antigen / metabolism*
  • Colitis, Ulcerative / chemically induced
  • Colitis, Ulcerative / metabolism
  • Colitis, Ulcerative / therapy*
  • Colon / immunology
  • Colon / metabolism
  • Cytokines / metabolism
  • Disease Models, Animal
  • Female
  • Genetic Therapy*
  • Mice, Inbred BALB C
  • Random Allocation
  • T-Lymphocytes / physiology
  • Trinitrobenzenesulfonic Acid

Substances

  • Carcinoembryonic Antigen
  • Ceacam1 protein, mouse
  • Cytokines
  • Trinitrobenzenesulfonic Acid