Total soluble and endogenous secretory receptor for advanced glycation endproducts (RAGE) in IBD

Meijer, Berrie; Hoskin, Teagan; Ashcroft, Anna; Burgess, Laura; Keenan, Jacqueline I.; Falvey, James D.; Gearry, Richard B.; Day, Andrew S.

doi:10.1016/j.crohns.2013.11.004

Cited by 14 publications

(17 citation statements)

References 37 publications

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“…Similar to inflammatory bowel disease in humans,136 serum sRAGE concentrations are significantly decreased in dogs with CIE but do not correlate with the severity of clinical signs, overall histologic lesions, or outcome 27. However, a weak correlation exists between serum sRAGE concentrations and histologic duodenal lesions (Cabrera Garcia, personal communication 2018).…”

Section: Biomarkers In Chronic Inflammatory Enteropathies Of Dogsmentioning

confidence: 99%

“…135 The lack of a correlation between serum sRAGE and S100A12 concentrations suggests that sRAGE is a nonspecific decoy receptor in dogs. 27 Similar to inflammatory bowel disease in humans, 136 [IL]-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p40, IL-17, IL-18, IL-23, IL-25, IL-33, IFN-γ, TNF-α, and TGF-β1) in dogs with CIE, [137][138][139][140][141][142][143] all of which do not support a Th1 nor Th2 polarization as described for inflammatory bowel diseases in humans. 144,145 There also is no evidence of a Th17 signature in dogs with CIE. 146,147 One problem with using cytokines as biomarkers in dogs is that there are many cytokine assays available.…”

Section: Soluble Receptor For Advanced Glycation End Productsmentioning

confidence: 99%

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Clinical utility of currently available biomarkers in inflammatory enteropathies of dogs

Heilmann

Steiner

2018

Veterinary Internal Medicne

108

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Chronic inflammatory enteropathies (CIE) in dogs are a group of disorders that are characterized by chronic persistent or recurrent signs of gastrointestinal disease and histologic evidence of mucosal inflammation. These CIEs are classified as either food‐responsive, antibiotic‐responsive, or immunosuppressant‐responsive enteropathy. Patients not clinically responding to immunomodulatory treatment are grouped as nonresponsive enteropathy and dogs with intestinal protein loss as protein‐losing enteropathy. Disease‐independent clinical scoring systems were established in dogs for assessment of clinical disease severity and patient monitoring during treatment. Histopathologic and routine clinicopathologic findings are usually not able to distinguish the subgroups of CIE. Treatment trials are often lengthy and further diagnostic tests are usually at least minimally invasive. Biomarkers that can aid in defining the presence of disease, site of origin, severity of the disease process, response to treatment, or a combination of these would be clinically useful in dogs with CIE. This article summarizes the following biomarkers that have been evaluated in dogs with CIE during the last decade, and critically evaluates their potential clinical utility in dogs with CIE: functional biomarkers (cobalamin, methylmalonic acid, folate, α1‐proteinase inhibitor, immunoglobulin A), biochemical biomarkers (C‐reactive protein, perinuclear anti‐neutrophilic cytoplasmic antibodies, 3‐bromotyrosine, N‐methylhistamine, calprotectin, S100A12, soluble receptor of advanced glycation end products, cytokines and chemokines, alkaline phosphatase), microbiomic biomarkers (microbiome changes, dysbiosis index), metabolomic biomarkers (serum metabolome), genetic biomarkers (genomic markers, gene expression changes), and cellular biomarkers (regulatory T cells). In addition, important performance criteria of diagnostic tests are briefly reviewed.

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Section: Biomarkers In Chronic Inflammatory Enteropathies Of Dogsmentioning

confidence: 99%

Section: Soluble Receptor For Advanced Glycation End Productsmentioning

confidence: 99%

Clinical utility of currently available biomarkers in inflammatory enteropathies of dogs

Heilmann

Steiner

2018

Veterinary Internal Medicne

108

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“…115 A number of small studies have attempted to correlate blood soluble RAGE levels with the presence and activity of IBD with conflicting results. 55,[116][117][118][119] In addition to RAGE, DAMP regulatory pathways may play a role in IBD. The TREM-1 (triggering receptor expressed on myeloid cells 1) is an immunoglobulin present on monocytes and neutrophils that upregulates DAMP-PRR-mediated signaling.…”

Section: Damp Pathways In Ibdmentioning

confidence: 99%

Gut mucosal DAMPs in IBD: from mechanisms to therapeutic implications

et al. 2016

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Endogenous damage-associated molecular patterns (DAMPs) are released during tissue damage and have increasingly recognized roles in the etiology of many human diseases. The inflammatory bowel diseases (IBD), ulcerative colitis (UC) and Crohn's disease (CD), are immune-mediated conditions where high levels of DAMPs are observed. DAMPs such as calprotectin (S100A8/9) have an established clinical role as a biomarker in IBD. In this review, we use IBD as an archetypal common chronic inflammatory disease to focus on the conceptual and evidential importance of DAMPs in pathogenesis and why DAMPs represent an entirely new class of targets for clinical translation.

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“…Because these isoforms lack a transmembrane domain, they are secreted and act as decoy receptors. Indeed, sRAGE has been shown to prevent or reverse RAGE signals in experimental models of diabetic atherosclerosis, wound healing, amyloidosis, and colitis 36 – 39 . In addition, Zhang and colleagues reported that sRAGE treatment significantly attenuates the neutrophilic inflammation and pathological changes in the LPS-induced murine model of acute lung injury, suggesting that sRAGE may be secreted as a decoy receptor and contributes to the suppression of excessive inflammatory responses during actual lung injury 40 .…”

Section: Discussionmentioning

confidence: 99%

sRAGE alleviates neutrophilic asthma by blocking HMGB1/RAGE signalling in airway dendritic cells

Zhang

Huang

et al. 2017

Sci Rep

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Receptor for advanced glycation end products (RAGE) plays a role in inflammatory reactions. The soluble form of RAGE (sRAGE) acts as a decoy to inhibit interactions of RAGE with advanced glycation end products such as High mobility group box 1 (HMGB1). We have demonstrated that HMGB1 directs Th17 skewing by regulating dendritic cell (DC) functions in a previous study. However, the protective effects of HMGB1 blockade with sRAGE in the development of neutrophilic asthma remain unclear. Here, we showed that allergen challenge decreased expression of sRAGE in a murine model of neutrophilic asthma, correlating well with neutrophil counts and interleukin (IL)-17 production. When HMGB1 signalling was blocked by intratracheal administration of sRAGE before sensitisation, HMGB1 expression, neutrophilic inflammation, and Th17-type responses were reduced significantly. Anti-asthma effects of sRAGE were achieved by inhibition of RAGE and IL-23 expression in airway CD11c+ antigen-presenting cells. Finally, we showed that sRAGE inhibited Th17 polarisation induced by recombinant HMGB1 (rHMGB1)-activated dendritic cells (DCs) in vitro. Adoptive transfer of rHMGB1-activated DCs was sufficient to restore airway inflammation, whereas transfer of rHMGB1 plus sRAGE-activated DCs significantly reduced neutrophilic inflammation. Thus, sRAGE prevents Th17-mediated airway inflammation in neutrophilic asthma at least partly by blocking HMGB1/RAGE signalling in DCs.

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Total soluble and endogenous secretory receptor for advanced glycation endproducts (RAGE) in IBD

Abstract: Although total sRAGE varied with activity in UC, esRAGE concentrations correlated inversely with endoscopic disease activity and CRP levels in both UC and CD. Additional studies are required to further define the significance of sRAGE and esRAGE in IBD.

Cited by 14 publications

References 37 publications

Clinical utility of currently available biomarkers in inflammatory enteropathies of dogs

Clinical utility of currently available biomarkers in inflammatory enteropathies of dogs

Gut mucosal DAMPs in IBD: from mechanisms to therapeutic implications

sRAGE alleviates neutrophilic asthma by blocking HMGB1/RAGE signalling in airway dendritic cells

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