Analysis of inflammatory signals in Japanese children with Crohn's disease

Pediatr Int. 2013 Dec;55(6):753-6. doi: 10.1111/ped.12159. Epub 2013 Aug 21.

Abstract

Background: Although it is recognized that the Th1 and Th17 cytokines are directly involved in the pathogenesis of Crohn's disease (CD), the precise cause of pediatric CD in the Japanese population has not been well established. In the present study, we examined the expression of pro-inflammatory cytokines and their signaling molecules in the intestinal mucosa of Japanese children with acute- and remission-phase CD.

Methods: A total of 11 children with acute-phase CD (mean age 10.32 ± 6.02 years) and 20 children with remission-phase CD (mean age 11.87 ± 4.29 years) provided samples for a serum cytokine assay. Among these children, seven with acute-phase CD (mean age 13.63 ± 1.94 years), six with remission-phase CD (mean age 9.93 ± 4.33 years), and six healthy controls (mean age 9.90 ± 4.88 years) provided samples for a signaling assay. Among this group, the expression of Th1, Th2, Th17, and regulatory T-cell signaling molecules were examined by real-time polymerase chain reaction.

Results: A significant elevation in the serum level of interleukin-6 and tumor necrosis factor-α was confirmed in pediatric patients with acute-phase CD compared to patients with remission-phase CD (P < 0.01 and 0.05, respectively). The mucosal expression of interferon-γ, signal transducer and activator of transcription 4, and transforming growth factor-β1 were significantly enhanced in pediatric patients with acute-phase CD compared to patients with remission-phase CD or those with normal mucosa.

Conclusions: These results suggest the possible involvement of Th1 and Th17 signaling in the pathogenesis of CD in Japanese children.

Keywords: Crohn's disease; Th1; Th17; interleukin-6; signal transducer and activator of transcription 4.

MeSH terms

  • Asian People
  • Child
  • Crohn Disease / immunology*
  • Cytokines / immunology*
  • Female
  • Humans
  • Male

Substances

  • Cytokines