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Published on: February 14, 2021
Analysis of inflammatory signals in Japanese children with Crohn's disease
Yoshito Fujitake1, Yoshikazu Ohtsuka, Tamaki Ikuse
1Department of Pediatrics and Adolescent Medicine, Juntendo University School of Medicine, Hongo, Tokyo; Department of Pediatrics, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
Insights
This study investigated Crohn
Area of Science:
- Immunology
- Gastroenterology
- Pediatrics
Background:
- Crohn's disease (CD) pathogenesis involves Th1 and Th17 cytokines.
- The exact cause of pediatric CD in Japan remains unclear.
- This study investigates pro-inflammatory cytokines in Japanese pediatric CD patients.
Purpose of the Study:
- To examine pro-inflammatory cytokine and signaling molecule expression in pediatric CD patients.
- To differentiate between acute and remission phases of pediatric CD in Japan.
- To explore the role of Th1 and Th17 signaling in pediatric CD pathogenesis.
Main Methods:
- Serum cytokine assays were performed on 11 acute-phase and 20 remission-phase pediatric CD patients.
- Intestinal mucosal samples were analyzed for signaling molecule expression via real-time PCR.
- Examined Th1, Th2, Th17, and regulatory T-cell signaling molecules in pediatric CD patients and controls.
Main Results:
- Elevated serum interleukin-6 and tumor necrosis factor-α in acute-phase pediatric CD patients.
- Increased mucosal expression of interferon-γ, STAT4, and TGF-β1 in acute-phase pediatric CD.
- Significant differences observed when comparing acute CD, remission CD, and healthy controls.
Conclusions:
- Th1 and Th17 signaling pathways are implicated in pediatric CD pathogenesis in Japan.
- Findings highlight the role of specific cytokines in acute pediatric CD.
- Further research is warranted to elucidate precise mechanisms.
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.
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