Inflammatory bowel disease

Yoshida, Hideo; Granger, D. Neil

doi:10.1002/ibd.20896

Cited by 114 publications

(52 citation statements)

References 69 publications

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“…In addition to RA, potential contribution of platelets and platelet-derived factors is also under consideration for inflammatory bowel disease (IBD), namely Crohn’s disease and ulcerative colitis (reviewed in detail elsewhere [87,88]). These disorders are known to be associated with an increased risk for thromboembolism [87].…”

Section: Rheumatoid Arthritismentioning

confidence: 99%

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The Inflammatory Role of Platelets: Translational Insights from Experimental Studies of Autoimmune Disorders

Pankratz

Bittner

Kehrel

et al. 2016

IJMS

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Beyond their indispensable role in hemostasis, platelets have shown to affect the development of inflammatory disorders, as they have been epidemiologically and mechanistically linked to diseases featuring an inflammatory reaction in inflammatory diseases like multiple sclerosis, rheumatoid arthritis and inflammatory bowel disorders. The identification of novel molecular mechanisms linking inflammation and to platelets has highlighted them as new targets for therapeutic interventions. In particular, genetic and pharmacological studies have identified an important role for platelets in neuroinflammation. This review summarizes the main molecular links between platelets and inflammation, focusing on immune regulatory factors, receptors, cellular targets and signaling pathways by which they can amplify inflammatory reactions and that make them potential therapeutic targets.

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Section: Rheumatoid Arthritismentioning

confidence: 99%

“…These disorders are known to be associated with an increased risk for thromboembolism [87]. Interestingly, there is evidence that patients suffering from IBD reveal a larger number but smaller size of platelets.…”

Section: Rheumatoid Arthritismentioning

confidence: 99%

The Inflammatory Role of Platelets: Translational Insights from Experimental Studies of Autoimmune Disorders

Pankratz

Bittner

Kehrel

et al. 2016

IJMS

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“…Patients with IBD exhibit a 3–6 fold higher risk for development of thromboembolism (TE) than the general population, with clinical studies suggesting an incidence of TE of approximately 6%, while autopsy studies predict an incidence as high as 40%. 5,6 Hematologic studies of IBD patients suggest that abnormalities in coagulation, fibrinolysis, and platelet function are likely to contribute to the prothrombogenic state that related to this disease 7 . These hematological changes as well as the enhanced thrombus formation reported in IBD patients have also been demonstrated in animal models of colitis 8,9 .…”

Section: Introductionmentioning

confidence: 99%

MyD88 Mediates the Protective Effects of Probiotics Against the Arteriolar Thrombosis and Leukocyte Recruitment Associated with Experimental Colitis

Souza

Senchenkova

Russell

et al. 2015

Inflammatory Bowel Diseases

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Several studies in IBD patients and in animal models of IBD have revealed a protective effect of probiotics in reducing clinical symptoms of disease and in blunting the gut inflammation that accompanies this condition. However, the mechanism underlying the therapeutic effect of probiotics is currently unknown. Furthermore, the ability of probiotics to influence the enhanced thrombus development that accompanies IBD has not been studied. This study addresses whether the enhanced extra-intestinal thrombosis (induced by light/dye injury) associated with experimental colitis is altered by oral treatment with the probiotic preparation VSL#3 or by the absence of microbiota. Colitis was induced by DSS 3% in Swiss Webster mice, germ free mice, C57BL/6 WT or Myd88−/− mice. In some experiments, mice received VSL#3 for 8 days before and during DSS feeding. Swiss Webster mice were also subjected to a chronic model of DSS colitis and the effect of VSL#3 was evaluated. VSL#3 treatment significantly attenuated the accelerated thrombus formation observed in both acute and chronic models of colitis. VSL#3-treated mice also exhibited attenuated inflammatory response and injury in the colon. The protective effects of VSL#3 on colitis-associated thrombogenesis and inflammation were not evident in MyD88-deficient mice. Our results suggest that improved control of the enteric microflora in IBD may afford protection against the hypercoagulable, prothrombotic state that follows this condition.

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“…ganciclovir) to reduce the severity of colonic injury. These results underscore the need for further investigation into the mechanisms underlying the impact of different phases of CMV infection on IBD, with some focus on how CMV might affect coagulation pathways and platelet responses [29, 30], and gut wall integrity [20], which are already perturbed during IBD. Less severe, more chronic models of colitis such as recently used by Matsumura et al [28] will be of benefit to enhance elucidation of the role of CMV in colitis.…”

Section: Discussionmentioning

confidence: 99%

The impact of primary and persistent cytomegalovirus infection on the progression of acute colitis in a murine model

Becker

Stokes

2015

Pathophysiology

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Cytomegalovirus (CMV) infects 60-100% of the population worldwide. CMV has been implicated in many diseases through the induction of inflammation. Inflammatory bowel disease (IBD) affects over 1 million Americans annually. IBD, in particular ulcerative colitis, has been associated with CMV infection. Here we use a murine model to test if both primary and persistent CMV infections exacerbate colitis. C57Bl/6J mice were injected with mock inoculum or murine CMV (mCMV) 4d (primary infection) or 6wks (persistent infection) before inducing colitis. Colitis was induced by administering 3% DSS (dextran sodium sulfate) in the drinking water for 6 days. Distilled water was given to controls. Disease activity index (DAI), derived from scores for stool consistency, body weight loss, occult blood, and rectal bleeding, was recorded daily. DAI increased early with DSS treatment in mocks when compared with water-treated controls. This was accelerated by both primary and persistent mCMV and appeared to be primarily due to the earlier appearance of gross bleeding versus their mock controls. Mocks reached similar DAI values by day 6. Myeloperoxidase was modestly elevated in the mCMV 4d-DSS over the mock 4d-DSS, however there was no such synergism in the 6 wk groups. Histology was comparable in mock and mCMV groups. Taken together our findings show that mCMV accelerated the development of acute colitis although a milder model of colitis may be needed to better delineate the impact of the virus on disease progression. Further work focusing on disruption of barrier function and bleeding may help determine the underlying mechanisms.

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Inflammatory bowel disease

Cited by 114 publications

References 69 publications

The Inflammatory Role of Platelets: Translational Insights from Experimental Studies of Autoimmune Disorders

The Inflammatory Role of Platelets: Translational Insights from Experimental Studies of Autoimmune Disorders

MyD88 Mediates the Protective Effects of Probiotics Against the Arteriolar Thrombosis and Leukocyte Recruitment Associated with Experimental Colitis

The impact of primary and persistent cytomegalovirus infection on the progression of acute colitis in a murine model

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