Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2019 Mar;17(3):2341-2348.
doi: 10.3892/etm.2019.7162. Epub 2019 Jan 9.

Aggravated mucosal and immune damage in a mouse model of ulcerative colitis with stress

Yanxia Gong  1 , Wei Niu  1 , Yanping Tang  1 , Qingyu Zhang  2 , Simiao Liu  1 , Xi Liu  1 , Xiao Wang  3 , Yang Xu  1
Affiliations

Aggravated mucosal and immune damage in a mouse model of ulcerative colitis with stress

Yanxia Gong et al. Exp Ther Med. 2019 Mar.

Abstract

The aim of the present study was to determine the influence of stress on the colonic mucosa and immune system and to further investigate the association between stress and development and pathogenesis of ulcerative colitis (UC). Mice were treated with 2,4,6-trinitrobenzenesulfonic acid to induce an animal model of UC, and stress was induced by water immersion and restraint. Subsequently, the disease activity index (DAI), secretory immunoglobulin A (sIgA), IgA, interleukin (IL)-6 and -8, tumor necrosis factor-α (TNF-α), complement component (C)3 and C4, and alterations in the colonic mucosa were observed. The DAI scores and the expression levels of IL-6, IL-8 and TNF-α significantly increased in the experimental UC mice compared with the control mice, while the expression levels of IgA and sIgA decreased (all P<0.01). DAI and colonic mucosa damage scores increased in the stress-treated mouse models of UC compared with the untreated mouse models of UC (P<0.05). Expression levels of IgA and sIgA decreased, while IL-6, IL-8 and TNF-α further increased in the stress-treated UC mice (P<0.05). The expression levels of C3 and C4 were not affected by stress or UC (P>0.05). These results indicated that UC may be associated with an immune disorder and that stress can aggravate colonic mucosa injury and alter the immune response. Furthermore, stress and immunity may serve roles in the pathogenesis of UC.

Keywords: immune response; injury; mice; mucosa; stress; ulcerative colitis.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
Body weight, disease activity index score and mucosa macroscopic and microscopic scores of mice. (A) The body weight of mice. (B) The disease activity index score score in group A, B, C and D. TNBS-ethanol solution was only administered in groups C and D (Establishment of the animal model of UC with TNBS-ethanol solution). (C) The macroscopic and microscopic scores of the colonic mucosa of mice. A (control group), B (stress group), C (UC and stress group), D (UC model alone). *P,0.05, **P<0.01. UC, ulcerative colitis.
Figure 2.
Figure 2.
Survival conditions of mice. A, control group; B, stress group; C, UC and stress group; D, UC model alone. The results demonstrated that the survival of mice after administration of TNBS-ethanol solution in group C was lower than group A (P=0.0455). However, there were no significant differences among groups B, C and D. UC, ulcerative colitis.
Figure 3.
Figure 3.
Macroscopic appearance of the colonic mucosa. (A) The external appearance of colonic tissue after excision in group A. (B) Section mucosal appearance of colonic tissue after incision in group A. (C) External appearance of colonic tissue after excision in group B. (D) Section mucosal appearance of colonic tissue after incision in group B. (E) External appearance of colonic tissue after excision in group C. (F) The section mucosal appearance of colonic tissue after incision in group C. (G) The external appearance of colonic tissue after excision in group D. (H) Section mucosal appearance of colonic tissue after incision in group D.
Figure 4.
Figure 4.
The microscopic appearance of the colonic mucosa. (A) control group; (B) stress group; (C) UC and stress group; (D) UC model alone. Observed under inverted microscopy at ×200 magnification. UC, ulcerative colitis.
Figure 5.
Figure 5.
The serum expression levels of IL-6, IL-8, TNF-α, C3, C4, IgA and sIgA in different groups. A, control group; B, stress group; C, UC and stress group; D, UC model alone. *P,0.05, **P<0.01. IL, interleukin; TNF, tumor necrosis factor; Ig, immunoglobulin; s, soluble; C, complement component; ns, not significant.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. DeRoche TC, Xiao SY, Liu X. Histological evaluation in ulcerative colitis. Gastroenterol Rep. 2014;2:178–192. doi: 10.1093/gastro/gou031. - DOI - PMC - PubMed
    1. Parente JM, Coy CS, Campelo V, Parente MP, Costa LA, da Silva RM, Stephan C, Zeitune JM. Inflammatory bowel disease in an underdeveloped region of Northeastern Brazil. World J Gastroenterol. 2015;21:1197–1206. doi: 10.3748/wjg.v21.i4.1197. - DOI - PMC - PubMed
    1. Shivashankar R, Tremaine WJ, Harmsen WS, Loftus EV., Jr Incidence and prevalence of crohn's disease and ulcerative colitis in olmsted county, minnesota from 1970 through 2010. Clin Gastroenterol Hepatol. 2017;15:857–863. doi: 10.1016/j.cgh.2016.10.039. - DOI - PMC - PubMed
    1. Kabi A, Nickerson KP, Homer CR, McDonald C. Digesting the genetics of inflammatory bowel disease: Insights from studies of autophagy risk genes. Inflamm Bowel Dis. 2012;18:782–792. doi: 10.1002/ibd.21868. - DOI - PMC - PubMed
    1. Guo AY, Stevens BW, Wilson RG, Russell CN, Cohen MA, Sturgeon HC, Thornton A, Giallourakis C, Khalili H, Nguyen DD, et al. Early life environment and natural history of inflammatory bowel diseases. BMC Gastroenterol. 2014;14:216. doi: 10.1186/s12876-014-0216-8. - DOI - PMC - PubMed