Improved assay for fecal calprotectin

Tøn, Hege; Brandsnes, Øystein; Dale, S.; Holtlund, Jostein; Skuibina, Eugenia; Schjønsby, H; Johne, Berit

doi:10.1016/s0009-8981(99)00206-5

Cited by 185 publications

(106 citation statements)

References 30 publications

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“…Altered stool composition has also been reported, with increased levels of fecal calprotectin, which is secreted by recruited neutrophils in the intestinal lining and has been proposed to be a marker of intestinal inflammation (103). Taken together, these data demonstrate a substantial subversion of physiological gut microbiome and a correlation between pathogenic intestinal flora and gut inflammation in HIV disease (102).…”

Section: Characterization Of Stool Microbes and Translocating Flora Imentioning

confidence: 74%

Microbial Translocation in the Pathogenesis of HIV Infection and AIDS

2013

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SUMMARYIn pathogenic simian immunodeficiency virus (SIV) and human immunodeficiency virus (HIV) infections, the translocation of microbial products from the gastrointestinal (GI) tract to portal and systemic circulation has been proposed as a major driver of the chronic immune activation that is associated with disease progression. Consistently, microbial translocation is not present in nonpathogenic SIV infections of natural host species.In vivostudies demonstrated that HIV/SIV-associated microbial translocation results from a series of immunopathological events occurring at the GI mucosa: (i) early and severe mucosal CD4+depletion, (ii) mucosal immune hyperactivation/persistent inflammation; (iii) damage to the integrity of the intestinal epithelium with enterocyte apoptosis and tight junction disruption; and (iv) subverted the gut microbiome, with a predominance of opportunistic bacteria. Directin situevidence of microbial translocation has been provided for SIV-infected rhesus macaques showing translocated microbial products in the intestinal lamina propria and distant sites. While the mechanisms by which microbial translocation causes immune activation remain controversial, a key pathogenic event appears to be innate immunity activation via Toll-like receptors and other pathogen recognition receptors. Accumulating clinical observations suggest that microbial translocation might affect HIV disease progression, response to therapy, and non-AIDS comorbidities. Given its detrimental effect on overall immunity, several interventions to prevent/block microbial translocation are currently under investigation as novel therapeutic agents for HIV/AIDS.

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Section: Characterization Of Stool Microbes and Translocating Flora Imentioning

confidence: 74%

Microbial Translocation in the Pathogenesis of HIV Infection and AIDS

2013

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“…Upon receipt, samples were either stored at 48C or 2808C and extracted within two days or three months, respectively. 43 F-Cp was measured using the EK-CAL (10-600 mg/g analytical range), PhiCal (Cat. # 6937) and Calprest (Cat.…”

Section: Sample Extraction and Measurement Of Faecal Calprotectinmentioning

confidence: 99%

“…37 F-Cp is also considered useful in the management of IBD as it is a reliable predictor of relapse, particularly in ulcerative colitis (UC), 38,39 and a marker of mucosal healing in response to therapy. 40,41 Calprotectin is resistant to both in vitro and in vivo degradation, is uniformly distributed in faeces and is stable for up to seven days at room temperature, 42,43 allowing stool samples to be posted to the laboratory for f-Cp analysis. Following sample extraction, f-Cp may be quantified using several different enzyme-linked immunosorbent assays (ELISAs) with identical manufacturer-recommended cut-off values for distinguishing IBD from IBS.…”

Section: Introductionmentioning

confidence: 99%

Between-assay variability of faecal calprotectin enzyme-linked immunosorbent assay kits

et al. 2012

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Background: Faecal calprotectin (f-Cp), a marker of intestinal inflammation, can be used to distinguish between functional and organic bowel disease. F-Cp, following extraction, is commonly quantified using enzyme-linked immunosorbent assays (ELISAs) but there are no data comparing the different f-Cp assays or sample extraction devices. We, therefore, evaluated and compared the performance of the Immunodiagnostik, Bü hlmann and Eurospital f-Cp ELISA assays as well as the Roche, Immunodiagnostik and ScheBo Biotech commercial faecal extraction devices. We also briefly report results from a pilot f-Cp external quality assurance (EQA) scheme. Methods: Imprecision, linearity, recovery, drift and limit of quantitation of the f-Cp assays were evaluated and between-assay variability assessed. The three commercial sample extraction devices were compared with the manual weighing method. Four faecal samples were distributed as part of a pilot EQA scheme to 15 laboratories using quantitative ELISA f-Cp assays. Results: The three f-Cp assays demonstrated adequate intra-/interbatch imprecision, linearity and recovery. The crosscomparison study and EQA data demonstrated that, for the same sample, the Bü hlmann assay reports up to 3.8 times higher f-Cp concentrations than the Immunodiagnostik and Eurospital assays. On average, the commercial extraction devices led to a 7.8-28.1% under-recovery of f-Cp in comparison to the manual weighing method. Conclusions: Laboratories should be aware of the lack of the assay standardization, as demonstrated by the between-assay variability. A comparison between f-Cp concentrations reported by these assays and clinical markers of disease severity is required in order to determine their diagnostic accuracy. The EQA scheme represents the first available programme for f-Cp.

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“…of the homogenate was transferred to a tube and centrifuged for 20 min, and the supernatant was collected and frozen at -20℃. Calprotectin was analyzed by enzymelinked immunosorbent assay (ELISA) [22] .…”

Section: Assessment Of Colon Macroscopic and Histological Damagementioning

confidence: 99%

Effect of probiotics on pro-inflammatory cytokines and NF-κB activation in ulcerative colitis

Hegazy

El-Bedewy²

2010

WJG

237

128

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AIM:To demonstrate the therapeutic effect of probiotics in patients with ulcerative colitis (UC), and their effect on inflammatory mediators and nuclear factor (NF)-κB activation in these patients. METHODS:Thirty patients with mild to moderate UC were randomly classified into two groups: sulfasalazine group, who received sulfasalazine 2400 mg/d; and probiotic group, who received sulfasalazine 2400 mg/d with probiotic. The patients were investigated before and after 8 wk of treatment with probiotic (Lactobacillus delbruekii and Lactobacillus fermentum ). Colonic activity of myeloperoxidase (MPO) was assayed with UV spectrophotometry, the colonic content of interleukin (IL)-6 was determined by enzyme-linked immunosorbent assay (ELISA), fecal calprotectin was determined by ELISA, and expression of NF-κB p65 and tumor necrosis factor (TNF)-α proteins in colonic tissue was identified by immunohistochemistry and reverse transcription polymerase chain reaction, respectively. RESULTS:At the start of the study, colonic mucosal injury and inflammation were demonstrated in UC patients by hematoxylin and eosin staining, and an increase in colonic MPO activity, fecal calprotectin, and expression of colonic TNF-α and NF-κB p65 proteins. The use of probiotic for 8 wk significantly ameliorated the inflammation by decreasing the colonic concentration of IL-6, expression of TNF-α and NF-κB p65, leukocyte recruitment, as demonstrated by a decrease in colonic MPO activity, and the level of fecal calprotectin compared to sulfasalazine group and the control group (P < 0.05). CONCLUSION:Oral supplementation with probiotics could be helpful in maintaining remission and preventing relapse of UC.

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Improved assay for fecal calprotectin

Cited by 185 publications

References 30 publications

Microbial Translocation in the Pathogenesis of HIV Infection and AIDS

Microbial Translocation in the Pathogenesis of HIV Infection and AIDS

Between-assay variability of faecal calprotectin enzyme-linked immunosorbent assay kits

Effect of probiotics on pro-inflammatory cytokines and NF-κB activation in ulcerative colitis

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