Inflammatory Bowel Disease: The Classic Gastrointestinal Autoimmune Disease

Kaistha, Abha; Levine, Jeremiah

doi:10.1016/j.cppeds.2014.10.003

Cited by 74 publications

(53 citation statements)

References 20 publications

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“…Inflammatory bowel disease including UC and CD is an idiopathic disease caused by a deregulated immune response to host intestinal microflora (29). Macrophages play an essential role for intestinal homeostasis and the pathology of IBD; recent studies have demonstrated that distinct macrophages populations of intestinal are responsible for their functional plasticity under different conditions (30).…”

Section: Discussionmentioning

confidence: 99%

CD169 Expressing Macrophage, a Key Subset in Mesenteric Lymph Nodes Promotes Mucosal Inflammation in Dextran Sulfate Sodium-Induced Colitis

Wang

Hao

et al. 2017

Front. Immunol.

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Inflammatory bowel disease (IBD) including Crohn’s disease (CD) and ulcerative colitis is a relapsing-remitting illness. Patients with long-standing extensive colitis are easy to develop colorectal cancer (CRC). The increasing incidence of IBD and a substantial increase in the risk of CRC make the necessity to pay more attention on the regulation of inflammation especially by specific macrophages subset. The present study reported that a key subset of sinus macrophage expressing CD169 in mesenteric lymph nodes (mLNs) played an essential role in promoting mucosal inflammation. The results revealed that the subset expressing CD169 in mLNs increased significantly during the dextran sulfate sodium (DSS)-induced colitis. The colitic symptoms were alleviated in CD169-diphtheria toxin receptor (DTR) mice at least partially due to the deletion of CD169+ macrophages in mLNs. In addition, the levels of inflammatory cytokines as well as the percentage of Th17 cells in mLNs from CD169-DTR mice were much lower than those from WT mice with DSS-induced colitis. Further experiment in vitro demonstrated that the supernatant from whole cells of mLNs or colon tissues could promote the production of inflammatory factors by mLN cells or colon tissues from CD169-DTR mice. These results could be explained by the cell sorting result that CD11b+CD169+ macrophages expressed higher level of inflammatory factors directly. All these data indicated that CD169+ sinus macrophage in mLNs played an essential role on regulating mucosal inflammation.

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Section: Discussionmentioning

confidence: 99%

CD169 Expressing Macrophage, a Key Subset in Mesenteric Lymph Nodes Promotes Mucosal Inflammation in Dextran Sulfate Sodium-Induced Colitis

Wang

Hao

et al. 2017

Front. Immunol.

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“…25 Australasian data indicate increasing incidence of PIBD, predominantly in children of European ancestry, with lower rates in indigenous populations. 26 In a community based healthcare delivery system in northern California, [32][33][34][35][36][37][38][39][40] problems, anemia and thrombocytosis had a sensitivity of 90.8% and a specificity of 80% for ulcerative colitis and Crohn's disease (n=103 IBD, 50 controls, screening test). 51 Infectious causes should be excluded using stool nucleic acid amplification tests or culture.…”

Section: Epidemiologymentioning

confidence: 99%

Diagnosis and management of inflammatory bowel disease in children

Oliveira

Monteiro

2017

BMJ

123

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Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are lifelong conditions that often begin in childhood. The implications of IBD are of particular importance in children because of the potential negative effects on growth, development, psychosocial function, and overall wellbeing. The key management strategy is to achieve sustained control of intestinal inflammation and monitor for potential complications of the disease and side effects of therapies. Overall, the evidence on the management of IBD in children is less extensive than in adults, but good quality multicenter studies and various guidelines and society consensus statements are available. This review summarizes the evidence on the pathophysiology, diagnosis, and approaches to management of children and adolescents with IBD.

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“…Crohn's disease (CD) is a chronic inflammatory granulomatous disease involving the whole digestive tract, and predominantly occurs at the end of the ileum and adjacent colon (Khanna and Raffals, 2017;Torres et al, 2017). The pathological changes of CD show a periodic and jumping distribution, and its pathogenesis may be closely related to heredity, immunity, environment, bacterial infection, mucosal regulation and so on (Kaistha and Levine, 2014;Mydock-McGrane et al, 2017;Rosen et al, 2017). CD is common in Europe and the United States with an annual incidence of 10.7/100, 000-20.2/100, 000, while the incidence of CD in Asia is relatively low.…”

Section: Introductionmentioning

confidence: 99%

Thalidomide Prevented and Ameliorated Pathogenesis of Crohn’s Disease in Mice via Regulation of Inflammatory Response and Fibrosis

Chen

Luo

et al. 2019

Front. Pharmacol.

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Crohn's disease (CD) is a chronic, relapsing form of inflammatory bowel disease, seriously threatening human health. Thalidomide has been used for the treatment of CD. However, the effects and the possible mechanisms of thalidomide on CD are still unclear. Herein, our study demonstrated that thalidomide protected colon mucosa against trinitrobenzene-sulfonic acid (TNBS)-induced injury, diminished inflammatory infiltration and levels of IFN-γ, IGF-1, IL-6, IL-17, TNF-α, while increased the levels of IL-10 and TGF-γ. Moreover, it reversed the intestinal fibrosis and inhibited the accumulated infiltration, down-regulated the expression of col1a2, col3a2, MMP-3, MMP-9, MMP-1, TGF-γ, α-SMA, but up-regulated the expression of TIMP-1 and Vimentin. Although it could be observed that the effect of thalidomide administration in modeling was better than after modeling, there was no statistical difference between the two groups. The present study provided evidence that the therapeutic effect of thalidomide alleviated the inflammatory response and damage of colon tissue, mainly by restoring the imbalance of TH17/Treg cells and inhibiting intestinal fibrosis in TNBS-induced mice colitis.

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Inflammatory Bowel Disease: The Classic Gastrointestinal Autoimmune Disease

Cited by 74 publications

References 20 publications

CD169 Expressing Macrophage, a Key Subset in Mesenteric Lymph Nodes Promotes Mucosal Inflammation in Dextran Sulfate Sodium-Induced Colitis

CD169 Expressing Macrophage, a Key Subset in Mesenteric Lymph Nodes Promotes Mucosal Inflammation in Dextran Sulfate Sodium-Induced Colitis

Diagnosis and management of inflammatory bowel disease in children

Thalidomide Prevented and Ameliorated Pathogenesis of Crohn’s Disease in Mice via Regulation of Inflammatory Response and Fibrosis

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