Recent Advances: The Imbalance of Cytokines in the Pathogenesis of Inflammatory Bowel Disease

Guan, Qingdong; Zhang, Jiguo

doi:10.1155/2017/4810258

Cited by 133 publications

(95 citation statements)

References 99 publications

(147 reference statements)

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“…Tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) play essential roles in the pathophysiology of inflammatory bowel disease [29,30]. They modulate mucosal immune system, alter epithelial integrity, and orchestrate neutrophil and macrophage infiltration and activation which result in colonic injury.…”

Section: International Journal Of Chronic Diseasesmentioning

confidence: 99%

Acetic Acid-Induced Ulcerative Colitis in Sprague Dawley Rats Is Suppressed by Hydroethanolic Extract ofCordia vigneiLeaves through Reduced Serum Levels of TNF-αand IL-6

Owusu

Obiri

Ainooson

et al. 2020

International Journal of Chronic Diseases

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Background. Ulcerative colitis (UC) is a recurrent inflammatory bowel disease (IBD) that causes long-lasting inflammation on the innermost lining of the colon and rectum. Leaf decoctions of Cordia vignei have been used in traditional medicine either alone or in combination with other plant preparations to treat the disease. Aim. In this study, we investigated the effect of hydroethanolic extract of Cordia vignei leaves (CVE) on acetic acid-induced UC in rats. Method. Male Sprague Dawley rats received oral treatment of either saline (10 ml/kg), sulfasalazine (500 mg/kg), or CVE (30-300 mg/kg) daily for 7 days. On day 4, colitis was induced by a single intrarectal administration of 500 μl of acetic acid (4% v/v). Rats were sacrificed on day 8 and colons were collected for histopathological examination. Blood was also collected for haematological assessment. Results. CVE significantly (P < 0.05) prevented colonic ulceration and reduced the inflammatory score. Serum levels of TNF-α and IL-6 were significantly reduced. Depletion of superoxide dismutase (SOD) and catalase (CAT) activities by acetic acid was significantly inhibited while lipid peroxidation indexed as malondialdehyde (MDA) level in the colon was reduced. However, loss of body weight was not significantly affected by treatment with CVE. Conclusion. This data suggest that CVE has a potential antiulcerative effect.

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Section: International Journal Of Chronic Diseasesmentioning

confidence: 99%

Acetic Acid-Induced Ulcerative Colitis in Sprague Dawley Rats Is Suppressed by Hydroethanolic Extract ofCordia vigneiLeaves through Reduced Serum Levels of TNF-αand IL-6

Owusu

Obiri

Ainooson

et al. 2020

International Journal of Chronic Diseases

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“…Similarly, in human studies, IL-10 is constitutively produced by healthy human colon explants, and depletion of IL-10 results in higher production of LPS-induced IFNγ, TNF, and IL-17, as well as increased epithelial damage and crypt loss [32]. In people with CD, IL-12, IL-23, and IL-1β are higher in the inflamed mucosa and serum compared to healthy controls [33,34]. IL-10 may be important to reduce inflammatory mediators and initiate remission in people with IBD.…”

Section: Discussionmentioning

confidence: 98%

Intravenous immunoglobulin (IVIg) or IVIg‐treated macrophages reduce DSS‐induced colitis by inducing macrophage IL‐10 production

et al. 2019

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Intravenous immunoglobulin (IVIg) is used to treat immune‐mediated diseases but its mechanism of action is poorly understood. We have reported that co‐treatment with IVIg and lipopolysaccharide activates macrophages to produce large amounts of anti‐inflammatory IL‐10 in vitro. Thus, we asked whether IVIg‐treated macrophages or IVIg could reduce intestinal inflammation in mice during dextran sulfate sodium (DSS)‐induced colitis by inducing macrophage IL‐10 production in vivo. Adoptive transfer of IVIg‐treated macrophages reduces intestinal inflammation in mice and collagen accumulation post‐DSS. IVIg treatment also reduces DSS‐induced intestinal inflammation and its activity is dependent on the Fc portion of the antibody. Ex vivo, IVIg induces IL‐10 production and reduces IL‐12/23p40 and IL‐1β production in colon explant cultures. Co‐staining tissues for mRNA, we demonstrate that macrophages are the source of IL‐10 in IVIg‐treated mice; and using IL‐10‐GFP reporter mice, we demonstrate that IVIg induces IL‐10 production by intestinal macrophages. Finally, IVIg‐mediated protection is lost in mice deficient in macrophage IL‐10 production (LysMcre+/−IL‐10fl/fl mice). Together, our data demonstrate a novel, in vivo mechanism of action for IVIg. IVIg‐treated macrophages or IVIg could be used to treat people with intestinal inflammation and may be particularly useful for people with inflammatory bowel disease, who are refractory to therapy.

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“…The importance of Treg cells are further highlighted by (i) increased inflammation due to loss of IL-10, (ii) increased colitis due to impaired transforming growth factor-beta one (TGF-β1) signal transduction, (iii) impaired Treg cell function due to mutations in CD25 and IL-10, and (iv) reduced inflammation in the gut of recombination activating gene 1 knock out (RAG1 KO) mice upon adoptive co-transfer of T cells and Treg cells. Therefore, it is immensely important to be able to identify the immune ingredients that tilt this precarious immune imbalance of TH17 versus Treg cells towards a cure pathway [14][15][16][17].…”

Section: Immunological Pathogenesis In Ibdmentioning

confidence: 99%

CCR6–CCL20 Axis in IBD: What Have We Learnt in the Last 20 Years?

Ranasinghe

Eri

2018

Gastrointestinal Disorders

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CC chemokine receptor 6 (CCR6) and its specific partner CC chemokine ligand 20 (CCL20) are known to play a pivotal role in intestinal inflammation. CCR6-associated inflammatory bowel disease (IBD) is already at the forefront of experimental inflammatory disease models, being the subject of numerous analytical studies. IBD is associated with two sub phenotypes, Crohn’s disease (CD) and ulcerative colitis (UC). Both these disease entities produce potent immune dysregulation followed by intense tissue damage within the gut mucosal system, initiating symptoms that are severely debilitating. Multiple causative factors are said to be responsible for IBD, but direct immune dysfunction is kindled by overplay of innate and adaptive immune responses produced against the luminal contents through the weakened or leaky gut epithelial barrier. Once immune homeostasis is not achieved by endogenous protective mechanisms, the self-assertive adaptive immunity mobilizes its various T and B cell cohorts, initializing their immune mechanisms by deploying the immune cells towards the site of infection. CCR6 and its unique solitary ligand CCL20 are small protein molecules that are abundantly expressed by T and B lymphocytes and act as chemotactic immune-modulatory envoys that help in the deployment of the effector lymphocyte arm of the immune system and produce two directly opposing outcomes in IBD. This dichotomous immunity consists of either immune tolerance or inflammation which then develops into a chronic state, remaining unresponsive to inherent immunity or targeted clinical therapy. In this review, we have identified large numbers of experimental studies that have employed both mouse models and clinical subjects spanning a period of nearly two decades and we have clustered these into 13 different groups. This review will provide greater understanding of the CCR6–CCL20 axis in IBD and identify gaps in the literature that can be filled in the future.

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Recent Advances: The Imbalance of Cytokines in the Pathogenesis of Inflammatory Bowel Disease

Cited by 133 publications

References 99 publications

Acetic Acid-Induced Ulcerative Colitis in Sprague Dawley Rats Is Suppressed by Hydroethanolic Extract ofCordia vigneiLeaves through Reduced Serum Levels of TNF-αand IL-6

Acetic Acid-Induced Ulcerative Colitis in Sprague Dawley Rats Is Suppressed by Hydroethanolic Extract ofCordia vigneiLeaves through Reduced Serum Levels of TNF-αand IL-6

Intravenous immunoglobulin (IVIg) or IVIg‐treated macrophages reduce DSS‐induced colitis by inducing macrophage IL‐10 production

CCR6–CCL20 Axis in IBD: What Have We Learnt in the Last 20 Years?

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