Dysregulation of mucosal immune response in pathogenesis of inflammatory bowel disease

Xu, Xiaorong; Liu, Changqin; Feng, Bai–Sui; Liu, Zhanju

doi:10.3748/wjg.v20.i12.3255

Cited by 193 publications

(163 citation statements)

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“…The final common pathway of this dysregulated immune activation is an abundant infiltration of immune cells in the intestinal mucosa [15,[35][36][37][38][39] . These cells were found to release excessive proinflammatory mediators that amplify the inflammatory cascade through the activation of mitogen-activated protein kinases (MAPK) and NF-κB.…”

Section: Cytokines Implicated In Ibdmentioning

confidence: 99%

Overview of cytokines and nitric oxide involvement in immuno-pathogenesis of inflammatory bowel diseases

Soufli

Toumi

Rafa

et al. 2016

WJGPT

278

193

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Section: Cytokines Implicated In Ibdmentioning

confidence: 99%

Overview of cytokines and nitric oxide involvement in immuno-pathogenesis of inflammatory bowel diseases

Soufli

Toumi

Rafa

et al. 2016

WJGPT

278

193

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“…IL-4 and IL-13) and Th-17 cytokines are elevated in areas of active disease in the mucosa of UC patients. 8,9 Under homeostatic conditions, a balance exists between the production of pro-inflammatory cytokines by CD4+ T cells and anti-inflammatory cytokines (e.g., IL-10) by Tregs. Evidence (in mice and humans) suggests that lacking Tregs can lead to IBD; however a clear association between a local deficit of Tregs or the presence of defective Tregs and IBD development has not been established.…”

Section: Introductionmentioning

confidence: 99%

The Intersection of TNF, IBD and the Microbiome

Jones-Hall

Nakatsu

2016

Gut Microbes

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Inflammatory bowel disease (IBD), comprised of Crohn's disease and ulcerative colitis, is a chronic inflammatory condition of multifactorial etiology and risk factors. Currently, one of the most effective treatments for IBD is the use of Tumor Necrosis Factor (TNF) functional inhibitor drugs, however, this treatment can cause adverse reactions and has a relatively large percentage of incomplete or non-responders. This lack of response may be related to differences in patients' gut microbiomes prior to and after disease initiation or treatment. Recent observations in our lab using a rodent model of IBD support the theory that TNF drives acute colitis, but also that the microbiome differs in association with TNF production and colitis severity. Studies such as this and others provide new insights into host-microbiome interactions associated with colitis that can lead to new therapies to prevent or treat the disease.

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“…In a more current study, a lower number of CD19+CD5+ blood cells were found in patients with inflammatory bowel diseases compared to healthy controls [33]. CD5+ cells can act as regulatory B cells expressing high levels of IL-10 and suppressing experimental inflammatory bowel diseases in murine models [34]. …”

Section: Discussionmentioning

confidence: 99%

B1a Lymphocytes (CD19+CD5+) Deficiency in Patients with Crohn’s Disease and Its Relation with Disease Severity

Gil-Borrás

García‐Ballesteros

Benet-Campos

et al. 2018

Dig Dis

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Background/Aims: B1a cells (CD19+CD5+) are considered elements of the innate immune system. The aim of this study was to evaluate the frequency of B1a cells in the peripheral blood of patients with Crohn’s disease (CD) and its relation with disease severity. Methods: In this prospective study, a total of 128 subjects (64 CD patients and 64 healthy controls) were studied. B1a cells in peripheral blood, CD Activity Index, and Simple Endoscopic Score of B1a cells were studied. Results: A significant decrease of B1a cells in peripheral blood was observed in patients with CD versus controls (p = 0.002), especially in perforating or penetrating patterns (p = 0.017). A lower frequency of B1a cells is related to increased endoscopic severity (Spearman’s Rho: –0.559, p = 0.004). The mean frequency of B1a cells in patients with pre- and post-study surgery was significantly lower than that in patients who did not undergo surgery (p = 0.050 and p = 0.026, respectively). Conclusions: The B1a cell count in peripheral blood is lower in CD patients. This decrease is directly related to the severity of the disease (penetrating or perforating, Simple Endoscopy Score and surgery complication). These results pointed to the fact that B1a cells play an important role in immune protection in CD.

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Dysregulation of mucosal immune response in pathogenesis of inflammatory bowel disease

Cited by 193 publications

References 0 publications

Overview of cytokines and nitric oxide involvement in immuno-pathogenesis of inflammatory bowel diseases

Overview of cytokines and nitric oxide involvement in immuno-pathogenesis of inflammatory bowel diseases

The Intersection of TNF, IBD and the Microbiome

B1a Lymphocytes (CD19+CD5+) Deficiency in Patients with Crohn’s Disease and Its Relation with Disease Severity

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