Atorvastatin Reduces Plasma Levels of Chemokine (CXCL10) in Patients with Crohn's Disease

Grip, Olof; Janciauskiene, Sabina

doi:10.1371/journal.pone.0005263

Cited by 65 publications

(51 citation statements)

References 52 publications

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“…89 In an interventional study of 10 patients with mild Crohn's disease, 13 weeks of treatment with atorvastatin decreased clinical and biochemical Crohn's disease activity. 90 In a large retrospective cohort study, patients with IBD who had been exposed to statins were less likely than patients who had not taken statins to need corticosteroids (HR 0.82, 95% CI 0.71-0.94), after adjustment for comorbidities, health-care utilization and the use of other diseasemodifying agents. 91 In patients with IBD, statins were also associated with a trend towards reduced risk of hospitalization (HR 0.88, 95% CI 0.74-1.05), IBD-related surgery (HR 0.80, 95% CI 0.63-1.02) and need for anti-TNF agents (HR 0.72, 95% CI 0.46-1.11).…”

Section: Statinsmentioning

confidence: 99%

Epidemiology, risk factors and management of cardiovascular diseases in IBD

Singh

Kullo

Pardi

et al. 2014

Nat Rev Gastroenterol Hepatol

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IBD is an established risk factor for venous thromboembolism. In the past few years, studies have suggested that patients with IBD might also be at an increased risk of coronary heart disease and stroke. The increased risk is thought to be similar to the level of risk seen in patients with other chronic systemic inflammatory diseases such as rheumatoid arthritis. The risk of developing these conditions is particularly increased in young adults with IBD, and more so in women than in men. Conventional cardiovascular risk factors are not over-represented in patients with IBD, so the increased risk could be attributable to inflammation-mediated atherosclerosis. Patients with IBD often have premature atherosclerosis and have biochemical and genetic markers similar to those seen in patients with atherosclerotic cardiovascular disease. The role of chronic inflammation in IBD-associated cardiovascular disease merits further evaluation. Particular attention should be given to the increased risk observed during periods of increased disease activity and potential modification of the risk by immunosuppressive and biologic therapies for IBD that can modify the disease activity. In addition, preclinical studies suggest that cardiovascular medications such as statins and angiotensin-converting enzyme inhibitors might also favourably modify IBD disease activity, which warrants further evaluation.

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Section: Statinsmentioning

confidence: 99%

Epidemiology, risk factors and management of cardiovascular diseases in IBD

Singh

Kullo

Pardi

et al. 2014

Nat Rev Gastroenterol Hepatol

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“…However, atorvastatin is the only statin that has been investigated in patients with active Crohn's disease. Although the studies involved a small number of patients, a clinical benefit was seen following treatment with the drug [90,91]. Larger randomized controlled trials are needed to confirm these preliminary results, as well as to investigate effects on fibrogenesis as a primary outcome.…”

Section: Experimental Therapeutic Targets In Intestinal Fibrosismentioning

confidence: 99%

Pathogenic aspects and therapeutic avenues of intestinal fibrosis in Crohn's disease

2015

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In Crohn's disease, one of the two major forms of inflammatory bowel diseases in human beings, persistent and chronic inflammation promotes fibrotic processes thereby facilitating formation of strictures, the most common indication for surgical intervention in this disorder. The pathogenesis of Crohn's disease-associated fibrosis is not fully understood, but variants of genes involved in the recognition of microbial components/products [e.g. CARD15 (caspase-activating recruitment domain 15) and ATG16L1 (autophagy-related 16-like 1)] are associated with this phenotype, and experimental evidence suggests that intestinal fibrosis results from an altered balance between deposition of ECM (extracellular matrix) and degradation of ECM by proteases. Studies have also contributed to identify the main phenotypic and functional alterations of cells involved in the fibrogenic process, as well as molecules that stimulate such cells to produce elevated amounts of collagen and other ECM-related proteins. In the present review, we assess the current knowledge about cellular and molecular mediators of intestinal fibrosis and describe results of recent studies aimed at testing the preventive/therapeutic effect of compounds in experimental models of intestinal fibrosis.

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“…176 An array of inducible/inflammatory chemokines such as CXCL 8 177 and CCL20 178 are upregulated in IBD, with early attempts to regulate chemokine levels in IBD patients in vivo showing promising results. 179 In addition to this, constitutive/homeostatic chemokines such as CXCL12 and CCL14 have also been shown to be dysregulated in IBD, 180,181 with others such as CCL25 and CCL28 involved in the trafficking of specific T-cell subsets in the small and large intestine respectively.…”

Section: Chemokinesmentioning

confidence: 99%

Function of the intestinal epithelium and its dysregulation in inflammatory bowel disease

Henderson

Limbergen

Schwarze

et al. 2011

Inflammatory Bowel Diseases

109

107

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The intestinal epithelium not only acts as a physical barrier to commensal bacteria and foreign antigens but is also actively involved in antigen processing and immune cell regulation. The inflammatory bowel diseases (IBDs) are characterized by inflammation at this mucosal surface with well-recognized defects in barrier and secretory function. In addition to this, defects in intraepithelial lymphocytes, chemokine receptors, and pattern recognition receptors promote an abnormal immune response, with increased differentiation of proinflammatory cells and a dysregulated relationship with professional antigen-presenting cells. This review focuses on recent developments in the structure of the epithelium, including a detailed account of the apical junctional complex in addition to the role of the enterocyte in antigen recognition, uptake, processing, and presentation. Recently described cytokines such as interleukin-22 and interleukin-31 are highlighted as is the dysregulation of chemokines and secretory IgA in IBD. Finally, the effect of the intestinal epithelial cell on T effector cell proliferation and differentiation are examined in the context of IBD with particular focus on T regulatory cells and the two-way interaction between the intestinal epithelial cell and certain immune cell populations.

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Atorvastatin Reduces Plasma Levels of Chemokine (CXCL10) in Patients with Crohn's Disease

Cited by 65 publications

References 52 publications

Epidemiology, risk factors and management of cardiovascular diseases in IBD

Epidemiology, risk factors and management of cardiovascular diseases in IBD

Pathogenic aspects and therapeutic avenues of intestinal fibrosis in Crohn's disease

Function of the intestinal epithelium and its dysregulation in inflammatory bowel disease

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