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Updated: Jan 23, 2026

Systematic Scoring Analysis for Intestinal Inflammation in a Murine Dextran Sodium Sulfate-Induced Colitis Model
Published on: February 14, 2021
Linear growth failure induced by systemic inflammation inhibiting IGF-1/IGFBP axis in rats with asymptomatic colitis
Xiaoyang Sheng1, Xueqing Sun2, Feng Li1
1Department of Children and Adolescents Health Care, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute for Pediatric Research, MOE-Shanghai Key Laboratory of Children's Environmental Health, No.1665, Kongjiang Road, Yangpu District, Shanghai, 200092, China.
Insights
Asymptomatic intestinal inflammation, or colitis, can stunt growth in children, even with adequate nutrition. This study reveals that the resulting systemic inflammation impacts growth by affecting the insulin-like growth factor (IGF) axis.
Area of Science:
- Pediatric Gastroenterology
- Inflammatory Bowel Disease Research
- Growth and Development Studies
Background:
- Poor sanitation in developing regions is linked to childhood growth retardation, potentially due to asymptomatic intestinal infections.
- This study investigates the mechanism by which subclinical intestinal inflammation inhibits growth.
Purpose of the Study:
- To explore the mechanism of intestinal inflammation in inhibiting linear growth in the context of asymptomatic colitis.
- To determine the role of systemic inflammation and hormonal changes in growth failure associated with colitis.
Main Methods:
- Forty-eight Wistar rats were divided into control, colitis (induced by trinitrobenzenesulphonic acid), and pair-fed groups.
- Linear growth, plasma hormone levels, and systemic cytokine levels were measured and compared among groups.
Main Results:
- Rats with colitis showed significantly reduced linear growth compared to controls.
- Colitis induced significant alterations in hormone and cytokine profiles, including increased TNF-α, IL-6, and IGFBP2, and decreased IGF-1 and IGFBP3.
- Calprotectin and NF-κB expression were also altered in the colitis group.
Conclusions:
- Asymptomatic colitis-induced systemic inflammation inhibits linear growth in rats.
- The insulin-like growth factor (IGF)/IGF binding protein axis is implicated in mediating growth inhibition by colitis.
Background:
Children in poor areas show significant growth retardation that does not improve with an adequate supply of energy and nutrients, which may be related to asymptomatic intestinal infection caused by poor sanitation. Our objective was to explore the mechanism of intestinal inflammation inhibiting growth in the setting of asymptomatic colitis.
Methods:
Forty-eight 3-week-old Wistar rats were randomly divided into three groups: the control group, colitis group (with asymptomatic colitis induced by 2.5% trinitrobenzenesulphonic acid) and pair-fed group (daily food intake matched to the pair in the colitis group). The linear growth was assessed, and the plasma levels of hormone and systemic cytokines were detected and compared by independent two-sample t-test or one-way ANOVA among groups.
Results:
At d5, the increases in the body length of the control, colitis and pair-fed groups were 1.65 ± 0.34 cm, 1.10 ± 0.30 cm and 1.38 ± 0.26 cm, respectively, and the increase in the body length in the colitis group was significantly less than that in the control group (P < 0.05). There were significant differences in the levels of hormone and cytokines among three groups (P < 0.05). Compared with the control group, rats in the colitis group exhibited linear growth failure, as well as higher expression of calprotectin, tumour necrosis factor-α, interleukin-6 and insulin-like growth factor binding protein 2, lower insulin-like growth factor-1 and insulin-like growth factor binding protein 3, and lower expression of nuclear factor kappa B in hepatocytes.
Conclusions:
In addition to undernutrition, the systemic inflammatory response caused by asymptomatic colitis may inhibit the linear growth of rats by its influence on the insulin-like growth factor/insulin-like growth factor binding protein axis.
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