Management of Crohn’s disease and ulcerative colitis

Ray, Christopher; Sagar, P. M.

doi:10.1016/j.mpsur.2020.04.003

Cited by 5 publications

(3 citation statements)

References 14 publications

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“…As an inflammatory disease of the gastrointestinal tract, UC is very difficult to cure (1) and the World Health Organization considers it a Modern Difficult Disease (16). Recurrence of the disease is common and usually accompanied with parenteral lesions which mainly occur in the lungs (6).…”

Section: Discussionmentioning

confidence: 99%

Tonifying-Qi-and-Detoxification Decoction attenuated injuries of colon and lung tissues in ulcerative colitis rat model via regulating NF-κB and p38MAPK pathway

Yan

Jiang

et al. 2022

Ann Transl Med

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Background: Tonifying-Qi-and-Detoxification Decoction (TQDD) is a Chinese medicine compound. This research probed the possible protective effects of TQDD on injuries of the colon and lung tissues in ulcerative colitis (UC) rat model. Methods: UC rat model was established by colon mucosal tissue sensitization combined with TNBSethanol. Ninety-six rats were randomly divided into normal control (NC), model, sulfasalazine (SASP), and TQDD (low, middle, and high dosages) groups. After 4 weeks intervention, all rats were sacrificed. The microstructure of lung tissue was observed using hematoxylin-eosin (HE) staining. Transmission electron microscope (TEM) was utilized to assess the ultrastructure change of alveolar epithelial type II cells (AEC-II). The mRNA expressions of Bax, Caspase 3, nuclear factor kappa B (NF-κB) and NF-κB inhibitor α (IKBα) in tissues were measured via quantitative reverse transcription PCR (qRT-PCR) assay. Western blotting and immunohistochemistry (IHC) were used to test p38MAPK, activating transcription factor 2 (ATF2), c-jun and c-fos expressions in tissues. Results: TQDD alleviated microstructure change of lung tissues, lung cell apoptosis and ultrastructure alterations of AEC-II in UC rat model. Moreover, TQDD suppressed activation of NF-κB pathway in colon and lung tissues. Besides, TQDD inhibited p38MAPK pathway in colon and lung tissues, as well as reduced ATF2, c-jun, and c-fos expressions in colon and lung tissues.Conclusions: This research confirmed the beneficial effect of TQDD on injuries of colon and lung tissues in UC rat model. TQDD attenuated injuries of lung and colon tissues in colon mucosal tissue sensitization combined with TNBS-ethanol-caused UC model via regulating NF-κB and p38MAPK pathways.

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Section: Discussionmentioning

confidence: 99%

Tonifying-Qi-and-Detoxification Decoction attenuated injuries of colon and lung tissues in ulcerative colitis rat model via regulating NF-κB and p38MAPK pathway

Yan

Jiang

et al. 2022

Ann Transl Med

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“…Two main clinical types of IBD are recognized, which are ulcerative colitis (UC) and Crohn's disease (CD) [1]. The inflammation in UC is restricted to the colon and rectum, while in CD it involves any part of the gastrointestinal tract in a non-continuous fashion [2]. Both types are chronic progressive inflammatory conditions that tend to have periods of relapses and remissions [3].…”

Section: Introductionmentioning

confidence: 99%

Roles of IL-17A and IL-23 in the Pathogenesis of Ulcerative Colitis and Crohn’s Disease

Abdul-Hussein

Ali

Al-Khalidi

et al. 2021

eijs

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Inflammatory bowel disease (IBD) is a chronic inflammatory disorder, the etiology and pathogenesis of which have been suggested to be influenced by cytokines. Two main clinical types of IBD are recognized, namely ulcerative colitis (UC) and Crohn's disease (CD). The present study examined serum levels of two cytokines (IL-17A and IL-23) in 60 IBD patients (30 UC and 30 CD) and 30 healthy controls. The levels were correlated with age, gender, cigarette-smoking status, disease duration, family history, disease extension, symptoms, extra-intestinal manifestations, and medication. The results depicted that IL-17A level was significantly higher in UC and CD patients compared to control (45.2 ± 23.3 and 47.5 ± 34.4 vs. 15.6 ± 7.5 pg/ml, respectively; p < 0.001). Serum level of IL-23 was similarly increased in UC and CD patients compared to control (64.1± 23.7 and 62.5 ± 27.3 vs. 25.2 ± 11.1 pg/ml, respectively). However, the level of both cytokines showed no significant variation between UC and CD patients (p = 0.713 and 0.777, respectively). Distributing UC and CD patients into subgroups according to some characteristics revealed that IL-17A level was significantly increased in UC male compared to female patients (57.3 ± 18.2 vs. 34.5 ± 22.5 pg/ml; p = 0.005). It was also significantly increased in smoker UC patients compared with non-smoker patients (51.9 ± 19.4 vs. 31.6 ± 25.5 pg/ml; p = 0.022). Smoker CD patients also showed a significantly increased level of IL-23 compared to non-smoker patients (72.7 ± 28.5 vs. 52.2 ± 22.6 pg/ml; p = 0.038). In the case of family history, IL-23 level was significantly decreased in UC patients with a family history of IBD compared to CD patients with a family history (84.5 ± 24.3 vs. 50.4 ± 17.0 pg/ml.; p = 0.042). In conclusion, the present data suggest a role for IL-17A and IL-23 in the etiology and pathogenesis of UC and CD.

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“…Two major phenotypes of IBD are clinically recognized: ulcerative colitis (UC) and Crohn's disease (CD). The inflammation in UC is restricted to the colon and rectum, while in CD, it involves any part of the gastrointestinal tract in a noncontinuous fashion [2]. Their clinical presentations are similar, but diarrhea and bleeding are most likely presented in UC, whereas watery diarrhea and vague symptoms are encountered in CD [3].…”

Section: Introductionmentioning

confidence: 99%

Susceptibility role of soluble HLA-G and HLA-G 14-bp insertion/deletion polymorphism in inflammatory bowel disease

Abdul-Hussein

Ali

Al-Khalidi

et al. 2020

Egypt J Med Hum Genet

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Background Inflammatory bowel disease (IBD) is a group of chronic inflammatory disorders of the gastrointestinal tract. It is fundamentally related to a dysregulated immune response in the intestinal mucosa against microbiota in genetically predisposed individuals. Among the genetic and immunological factors that are suggested to have role in etiology and pathogenesis of IBD are human leukocyte antigen (HLA)-G molecules. Therefore, soluble HLA-G (sHLA-G) serum level and genetic association with HLA-G 14-bp insertion (Ins)/deletion (Del) polymorphism was analyzed in 100 IBD patients; 50 ulcerative colitis (UC) and 50 Crohn’s disease (CD), and 100 controls. Results sHLA-G level was significantly elevated in IBD patients compared to controls (174.7 ± 27.1 vs. 126.8 ± 15.1; corrected probability [pc] < 0.001). The level was also elevated in UC patients compared to CD patients but the difference was not significant (180.5 ± 27.1 vs. 168.9 ± 26.3; p = 0.059). Receiver operating characteristic analysis confirmed the significance of sHLA-G in total IBD, UC, and CD patients (area under curve = 0.944, 0.961, and 0.927, respectively). The genetic association was analyzed under five genetic models (allele, recessive, dominant, overdominant, and codominant). At the allele level, Del allele frequency was significantly increased in total IBD patients (Odds ratio [OR] = 1.93; 95% confidence interval [CI] = 1.27–2.94; pc = 0.018) and CD patients (OR = 2.08; 95% CI = 1.23–3.54; pc = 0.042) compared to controls. Among UC patients, a similar increased frequency was observed, but the pc value was not significance (OR = 1.79; 95% CI = 1.07–3.00; p = 0.031). At the genotypic level, Del/Del genotype was associated with a significantly increased IBD-risk in total patients under codominant model (OR = 4.06; 95% CI = 1.56–10.56; pc = 0.024). sHLA-G level was not influenced by the Ins/Del polymorphism. Conclusions This study demonstrated a significant increase in serum level of sHLA-G in UC and CD patients. Further, HLA-G 14-bp Ins/Del polymorphism may be associated with susceptibility to IBD, particularly CD.

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Management of Crohn’s disease and ulcerative colitis

Cited by 5 publications

References 14 publications

Tonifying-Qi-and-Detoxification Decoction attenuated injuries of colon and lung tissues in ulcerative colitis rat model via regulating NF-κB and p38MAPK pathway

Tonifying-Qi-and-Detoxification Decoction attenuated injuries of colon and lung tissues in ulcerative colitis rat model via regulating NF-κB and p38MAPK pathway

Roles of IL-17A and IL-23 in the Pathogenesis of Ulcerative Colitis and Crohn’s Disease

Susceptibility role of soluble HLA-G and HLA-G 14-bp insertion/deletion polymorphism in inflammatory bowel disease

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