scholarly journals Advances in In-Vivo Imaging of Inflammatory Bowel Disease Mediators

Author(s):  
Nicole Dmochowska ◽  
Hannah R. Wardill ◽  
Patrick A. Hughes

Inflammatory Bowel Disease (IBD) is characterized by chronic remitting and relapsing inflammation of the lower gastrointestinal tract. The etiology underlying IBD remains unknown but is thought to involve a hypersensitive immune response to environmental antigen, including the microbiota. Diagnosis and monitoring of disease is heavily reliant on endoscopy, which is invasive and does not provide information regarding specific mediators. This review describes recent developments in imaging of IBD with a focus on PET and SPECT imaging of inflammatory mediators, and how this may be applied to the microbiota.

2003 ◽  
Vol 1 (2) ◽  
pp. 65-71 ◽  
Author(s):  
M. Hatzistilianou-Sidiropoulou ◽  
S. Nousia-Arvanitakis ◽  
A. Galli-Tsinopoulou ◽  
C. Agguridaki ◽  
M. Xefteri ◽  
...  

Inflammatory bowel disease (IBD) in children remains a challenging problem. Crohn disease and ulcerative colitis are characterized by an activation of intestinal mononuclear cells and T-cells within the inflammed lesions. In the present study, we determined whether circulating inflammatory mediators, such as interleukins and adhesion molecules, may represent useful markers of immune activation in vivo. Serum concentrations of IL-2, IL-6, IL-8, IL-10, sIL-2R, sICAM-1 and sVCAM-1 were measured by a quantitative enzyme-linked immunosorbent assay (ELISA) in 18 patients with IBD and 25 healthy subjects matched for age and sex (control group). According to our results, all the inflammatory mediators are significantly increased in patients with IBD as compared to the control group. Pro-inflammatory mediators (IL-6, IL-8, IL-10) are elevated in the serum of patients with active disease, suggesting that they act as naturally occuring initiators of the acute inflammatory process. Increased IL-2 and sIL-2R levels reflect T-cell activation. Increased circulating sICAM-1 and sVCAM-1 levels may reflect increased adhesiveness and signal transmission across cells, probably as a result of shedding of the parent molecule during local cellular immunoresponses in vivo. The measurement of inflammatory mediators may be a useful adjunct to the clinical assessment and to the routine laboratory testing of IBD pediatric patients.


2002 ◽  
Vol 88 (S1) ◽  
pp. s5-s9 ◽  
Author(s):  
Fergus Shanahan

Probiotic therapy is attracting the renewed interest of clinicians and basic investigators from a variety of traditional research disciplines. While the theoretical rationale for modifying the commensal flora of the gastrointestinal tract in specific circumstances appears sound and requires scientific pursuit, the field of probiotics has been clouded by exaggerated claims from some quarters. In general, many of the claims for therapeutic efficacy have not been well substantiated, but the field is now poised for evaluation within the realm of evidence-based medicine. Alterations in commensal bacterial flora within the gastrointestinal tract are associated with susceptibility to pathogens such as Clostridium difficile and there is persuasive evidence that the normal flora may participate in the pathogenesis of inflammatory bowel disease and other chronic diseases in genetically susceptible individuals. This has prompted various strategies to fortify or otherwise modify the enteric flora by dietary supplements containing probiotic formulations. Detailed comparisons of probiotic performance amongst different bacterial strains have not been performed in vivo in man or under clinical trial conditions, and the level of scientific characterisation of individual organisms has been variable. In addition, it cannot be assumed that the same probiotic is equally suitable for all individuals. Moreover, the heterogeneity of clinical disorders such as Crohn's disease and ulcerative colitis implies that strain-specific properties may be required for subset-specific categories of patients. While cocktails of probiotics offer convenience, therapeutic progress may require clarification of the mechanism of probiotic action and may be delayed until individual bacterial components have been rigorously studied. More importantly, the full potential of therapeutic manipulation of the enteric flora with probiotics or other strategies may not be optimally realised until the composition and metabolic activities of the normal flora are better understood.


2018 ◽  
Vol 6 (5) ◽  
pp. 809-815 ◽  
Author(s):  
Wanfu Xu ◽  
Liying He ◽  
Qi Xia ◽  
Chunhong Jia ◽  
Lanlan Geng ◽  
...  

Inflammatory bowel disease (IBD) is a group of chronic remittent or progressive inflammatory gastrointestinal tract diseases, accompanying impaired barrier function.


2011 ◽  
Vol 140 (5) ◽  
pp. S-274
Author(s):  
Gianluca Andrisani ◽  
Daniela Frasca ◽  
Alessandro Armuzzi ◽  
Alfredo Papa ◽  
Manuela Marzo ◽  
...  

2021 ◽  
Author(s):  
Xiao fan Song ◽  
Lei Qiao ◽  
Shuqi Yan ◽  
Yue Chen ◽  
Xina Dou ◽  
...  

Selenium (Se) as an essential micronutrient that has implications in human diseases, including inflammatory bowel disease (IBD), especially with respect to Se deficiencies. Recently, selenium nanoparticles (SeNPs) have attracted significant...


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rayko Evstatiev ◽  
Adam Cervenka ◽  
Tina Austerlitz ◽  
Gunther Deim ◽  
Maximilian Baumgartner ◽  
...  

AbstractInflammatory bowel disease is a group of conditions with rising incidence caused by genetic and environmental factors including diet. The chelator ethylenediaminetetraacetate (EDTA) is widely used by the food and pharmaceutical industry among numerous other applications, leading to a considerable environmental exposure. Numerous safety studies in healthy animals have revealed no relevant toxicity by EDTA. Here we show that, in the presence of intestinal inflammation, EDTA is surprisingly capable of massively exacerbating inflammation and even inducing colorectal carcinogenesis at doses that are presumed to be safe. This toxicity is evident in two biologically different mouse models of inflammatory bowel disease, the AOM/DSS and the IL10−/− model. The mechanism of this effect may be attributed to disruption of intercellular contacts as demonstrated by in vivo confocal endomicroscopy, electron microscopy and cell culture studies. Our findings add EDTA to the list of food additives that might be detrimental in the presence of intestinal inflammation, but the toxicity of which may have been missed by regulatory safety testing procedures that utilize only healthy models. We conclude that the current use of EDTA especially in food and pharmaceuticals should be reconsidered. Moreover, we suggest that intestinal inflammatory models should be implemented in the testing of food additives to account for the exposure of this primary organ to environmental and dietary stress.


2018 ◽  
Vol 5 (3) ◽  
pp. 180107 ◽  
Author(s):  
Sophie C. Payne ◽  
Robert K. Shepherd ◽  
Alicia Sedo ◽  
James B. Fallon ◽  
John B. Furness

Inflammatory damage to the bowel, as occurs in inflammatory bowel disease (IBD), is debilitating to patients. In both patients and animal experimental models, histological analyses of biopsies and endoscopic examinations are used to evaluate the disease state. However, such measurements often have delays and are invasive, while endoscopy is not quantitatively objective. Therefore, a real-time quantitative method to assess compromised mucosal barrier function is advantageous. We investigated the correlation of in vivo changes in electrical transmural impedance with histological measures of inflammation. Four platinum (Pt) ball electrodes were placed in the lumen of the rat small intestine, with a return electrode under the skin. Electrodes placed within the non-inflamed intestine generated stable impedances during the 3 h testing period. Following an intraluminal injection of 2,4,6-trinitrobenzene sulfonic acid (TNBS), an established animal model of IBD, impedances in the inflamed region significantly decreased relative to a region not exposed to TNBS ( p  < 0.05). Changes in intestinal transmural impedance were correlated ( p  < 0.05) with histologically assessed damage to the mucosa and increases in neutrophil, eosinophil and T-cell populations at 3 h compared with tissue from control regions. This quantitative, real-time assay may have application in the diagnosis and clinical management of IBD.


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