Literature review in cases with exacerbation of ulcerative colitis induced by treatment with interferon and/or ribavirin

Watanabe, Takuya; Hirono, Haruka; Hasegawa, Katsuhiko; Soga, Kenji; Shibasaki, Koichi

doi:10.1111/j.1440-1746.2011.06890.x

Cited by 15 publications

(6 citation statements)

References 29 publications

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“…Given that type I IFNs has been used for the treatment of viral hepatitis and multiple sclerosis, and some patients suffer from ulcerative colitis (UC) and celiac disease during type I IFN treatment 33,34 the chronic IFN treatment may induce weakening of the IECs themselves by reducing stemness in addition to excessive activation of the immune system, leading to the development of these diseases.…”

Section: Discussionmentioning

confidence: 99%

IRF2 maintains the stemness of colonic stem cells by limiting physiological stress from interferon

Minamide

Sato

Nakanishi

et al. 2020

Sci Rep

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The physiological stresses that diminish tissue stem-cell characteristics remain largely unknown. We previously reported that type I interferon (IFN), which is essential for host antiviral responses, is a physiological stressor for hematopoietic stem cells (HSCs) and small intestinal stem cells (ISCs) and that interferon regulatory factor-2 (IRF2), which attenuates IFN signaling, maintains their stemness. Here, using a dextran sodium sulfate (DSS)-induced colitis model, we explore the role of IRF2 in maintaining colonic epithelial stem cells (CoSCs). In mice with a conditional Irf2 deletion in the intestinal epithelium (hereafter Irf2ΔIEC mice), both the number and the organoid-forming potential of CoSCs were markedly reduced. Consistent with this finding, the ability of Irf2ΔIEC mice to regenerate colon epithelium after inducing colitis was severely impaired, independently of microbial dysbiosis. Mechanistically, CoSCs differentiated prematurely into transit-amplifying (TA) cells in Irf2ΔIEC mice, which might explain their low CoSC counts. A similar phenotype was induced in wild-type mice by repeated injections of low doses of poly(I:C), which induces type I IFN. Collectively, we demonstrated that chronic IFN signaling physiologically stresses CoSCs. This study provides new insight into the development of colitis and molecular mechanisms that maintain functional CoSCs throughout life.

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Section: Discussionmentioning

confidence: 99%

IRF2 maintains the stemness of colonic stem cells by limiting physiological stress from interferon

Minamide

Sato

Nakanishi

et al. 2020

Sci Rep

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“…Others have suggested that the cytokine profile for UC is less defined, and includes both Th1 and Th2 cytokines (Fuss et al , 2004). Therefore, a Th1/Th2 imbalance is thought to be involved (Watanabe et al , 2011). Recently, several studies have highlighted the role of Th17 and its related cytokines in UC, where they elicit potent inflammatory responses (Shen & Durum, 2010; Strober & Fuss, 2011).…”

Section: Discussionmentioning

confidence: 99%

Interactions between Trichinella spiralis infection and induced colitis in mice

et al. 2013

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Inflammatory bowel disease (IBD) is a chronic relapsing inflammation afflicting any part of the bowel wall as a result of a deregulated and inappropriate immune response. In recent years, experimental and clinical evidence has demonstrated that infection with parasitic worms could protect hosts from IBD. The aims of this study were to determine if the underlying mechanism of the host immune regulation inherent to Trichinella spiralis infection involves Foxp3-expressing regulatory T cells, and to gain insight about time-related interactions between intestinal nematode infection and induced colitis using an experimental model for ulcerative colitis. Mice were experimentally subjected to acetic acid-induced colitis, which was either preceded or followed by T. spiralis infection. Assessment of colitis was done by histopathological examination of the colon and determination of pentraxin 3 levels. Immunohistochemistry was done for demonstration of Foxp3-expressing regulatory T cells in colonic tissues. It was evident that T. spiralis infection ameliorated the severe inflammation induced by acetic acid, evidenced by amelioration of histopathological changes and diminution of pentraxin 3 levels. The amelioration was more pronounced when T. spiralis infection preceded the induction of colitis. Regarding the immunohistochemical staining of regulatory T cells, T. spiralis infection induced recruitment of Foxp3-expressing regulatory T cells to areas of inflammation. In conclusion, T. spiralis regulatory mechanism can improve inflammation of the colon through the ‘inflammatory–regulatory’ axis. Finally, it would be of great importance to apply these results to the development of new therapeutic approaches for the treatment of ulcerative colitis.

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“…IFN-α/β also plays a role in the modulation of Th1 responses and it inhibits production of Th2 cytokines, IL-5 and IL-13 that are upregulated in the mucosa of UC patients [58]. However, the majority of patients treated with IFN-α/β experienced adverse events such as headache, arthralgia, myalgia, abdominal pain, fatigue and vomiting [59].…”

Section: The Role Of Biomarkers and Treatment Options In Ucmentioning

confidence: 99%

Ulcerative colitis: understanding its cellular pathology could provide insights into novel therapies

Kaur

Goggolidou

2020

J Inflamm

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Dynamic interactions between the gastrointestinal epithelium and the mucosal immune system normally contribute to ensuring intestinal homeostasis and optimal immunosurveillance, but destabilisation of these interactions in genetically predisposed individuals can lead to the development of chronic inflammatory diseases. Ulcerative colitis is one of the main types of inflammatory diseases that affect the bowel, but its pathogenesis has yet to be completely defined. Several genetic factors and other inflammation-related genes are implicated in mediating the inflammation and development of the disease. Some susceptibility loci associated with increased risk of ulcerative colitis are found to be implicated in mucosal barrier function. Different biomarkers that cause damage to the colonic mucosa can be detected in patients, including perinuclear ANCA, which is also useful in distinguishing ulcerative colitis from other colitides. The choice of treatment for ulcerative colitis depends on disease severity. Therapeutic strategies include anti-tumour necrosis factor alpha (TNF-α) monoclonal antibodies used to block the production of TNF-α that mediates intestinal tract inflammation, an anti-adhesion drug that prevents lymphocyte infiltration from the blood into the inflamed gut, inhibitors of JAK1 and JAK3 that suppress the innate immune cell signalling and interferons α/β which stimulate the production of anti-inflammatory cytokines, as well as faecal microbiota transplantation. Although further research is still required to fully dissect the pathophysiology of ulcerative colitis, understanding its cellular pathology and molecular mechanisms has already proven beneficial and it has got the potential to identify further novel, effective targets for therapy and reduce the burden of this chronic disease.

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Literature review in cases with exacerbation of ulcerative colitis induced by treatment with interferon and/or ribavirin

Cited by 15 publications

References 29 publications

IRF2 maintains the stemness of colonic stem cells by limiting physiological stress from interferon

IRF2 maintains the stemness of colonic stem cells by limiting physiological stress from interferon

Interactions between Trichinella spiralis infection and induced colitis in mice

Ulcerative colitis: understanding its cellular pathology could provide insights into novel therapies

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