Comparison of 4 Neutrophil-Derived Proteins in Feces As Indicators of Disease Activity in Ulcerative Colitis

Langhorst, Jost; Elsenbruch, Sigrid; Mueller, T.; Rueffer, Andreas; Spahn, G.; Michalsen, Andreas; Dobos, Gustav

doi:10.1097/01.mib.0000187980.08686.18

Cited by 130 publications

(96 citation statements)

References 34 publications

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“…In human studies, measurement of neutrophil markers, including MPO and other granule proteins and chemokines, in fecal contents and intestine lavage, is used for diagnosis and to monitor therapy and correlate well with other parameters, such as endoscopic grade of inflammation [41][42][43][44][45][46]. In mice, macrophages do not express MPO; only neutrophils do [47,48].…”

Section: Altered Neutrophil Influx In Mmp7 −/− Micementioning

confidence: 99%

Matrix metalloproteinase-7 (matrilysin) controls neutrophil egress by generating chemokine gradients

Swee

Wilson

Wang

et al. 2008

Journal of Leukocyte Biology

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Matrilysin [matrix metalloproteinase 7 (MMP7)] is induced by mucosal injury of many tissues. To assess function of this proteinase, we subjected wild-type and Mmp7 −/− mice to acute colon injury. When matrilysin expression was increasing, 73% of wild-type mice died, whereas only 32% of Mmp7 −/− mice succumbed. Although re-epithelialization was delayed in Mmp7 −/− mice, overall injury did not differ markedly between genotypes. We hypothesized that differences in acute inflammation caused increased mortality in wild-type mice. Indeed, whereas overall neutrophil influx into tissue was similar in wild-type and Mmp7 −/− mice, their location and extent of migration differed between genotypes. Neutrophils were dispersed throughout the mucosa and within the lumen of wild-type mice, but these leukocytes were largely confined to the submucosa in Mmp7 −/− mice. The levels of neutrophil chemokines, keratinocyte-derived chemokine and MIP-2, increased in the colon tissue of both genotypes, but these factors were detected only in lumenal lavages of wild-type mice. Our findings indicate that matrilysin mediates beneficial and deleterious effects in response to injury. On one hand, it promotes re-epithelialization, but it also controls the transepithelial influx of neutrophils, which if excessive, can lead to tissue damage.

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Section: Altered Neutrophil Influx In Mmp7 −/− Micementioning

confidence: 99%

Matrix metalloproteinase-7 (matrilysin) controls neutrophil egress by generating chemokine gradients

Swee

Wilson

Wang

et al. 2008

Journal of Leukocyte Biology

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“…In patients with lower gastrointestinal symptoms, faecal calprotectin and lactoferrin have been found to be equally recommendable. 13 Lactoferrin is more stable than calprotectin 14 and may be the marker of choice where delay in transit to the laboratory is anticipated.…”

Section: Introductionmentioning

confidence: 99%

Age-related faecal calprotectin, lactoferrin and tumour M2-PK concentrations in healthy volunteers

et al. 2009

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Editorial comment: Readers should be aware that the content of this research paper has changed substantially from the version that was originally published on-line on 9 September 2009. A reappraisal of the data has resulted in substantial changes to the originally quoted reference ranges. One author of the originally posted article has disassociated herself from this final version of the paper. AbstractObjective: Measurement of the faecal markers calprotectin, lactoferrin and tumour M2-PK has been reported to be useful in the diagnosis and management of a range of gastrointestinal disorders in both children and adults. The aim of this study was to investigate the requirement for age-related reference ranges. Methods: Faecal samples were obtained from 132 healthy subjects and analysis of calprotectin, lactoferrin and tumour M2-PK performed using commercially available enzyme-linked immunosorbent assay. Results: In the healthy subjects median concentrations were as follows: for calprotectin -2-9 y, 34 mg/g, 10-59 y, 22 mg/g and 60 y, 27 mg/g; for lactoferrin -2 -9 y, 2.2 mg/g, 10 y, 0.5 mg/g; and for tumour M2-PK all subjects ,1 U/mL. Significant differences between age groups for different markers resulted in the following age-related reference ranges: calprotectin -2 -9 y, ,166 mg/g, 10-59 y, ,51 mg/g, 60 y, ,112 mg/g; lactoferrin -2 -9 y, ,29 mg/g, 10 y ,4.6 mg/g. Conclusion:In healthy individuals, we found there to be variation in the faecal inflammatory markers calprotectin and lactoferrin with age. For both calprotectin and lactoferrin children aged 2-9 y had significantly higher concentrations than subjects aged 10 y. For calprotectin but not lactoferrin, adults 60 years had a higher concentration than those aged 10-59 y. There was no change with age in the metabolomic marker faecal tumour M2-PK in healthy subjects. The knowledge of age-related reference ranges in healthy subjects is important to fully interpret changes in gastrointestinal disease.

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“…Furthermore, stool samples of 7 patients and serum samples of 11 patients (stool sample size = 10; serum sample size = 34) were collected at the onset of GvHD and in the further progression of GvHD every 2-14 d. S100A8/ S100A9 concentrations in the stool were determined using calprotectin assay (Buehlmann). For S100A12 detection, ∼100 mg stool samples were suspended in extraction buffer at 1:50 dilution for homogenization, as described and validated previously (34,39,40). Concentrations of S100A8/ S100A9 and S100A12 in the serum were determined by double-sandwich ELISA, as described previously (34,41).…”

Section: S100 Elisamentioning

confidence: 99%

Monocyte-Induced Development of Th17 Cells and the Release of S100 Proteins Are Involved in the Pathogenesis of Graft-versus-Host Disease

Reinhardt

Foell

Vogl³

et al. 2014

The Journal of Immunology

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Graft-versus-host disease (GvHD) is a major cause of morbidity and mortality after allogeneic hematopoietic cell transplantation. However, the pathophysiology of GvHD remains poorly understood. In this study, we analyzed the induction of Th17 cells by monocytes of patients with GvHD in vitro, demonstrating that monocytes isolated from patients with acute skin and intestinal GvHD stage I–IV and chronic GvHD induce significantly increased levels of Th17 cells compared with patients without GvHD. S100 proteins are known to act as innate amplifier of inflammation. We therefore investigated the presence of S100 proteins in the stool, serum, and bowel tissue of patients with GvHD and the influence of S100 proteins on the induction of Th17 cells. Elevated levels of S100 proteins could be detected in patients with acute GvHD, demonstrating the release of these phagocyte-specific proteins during GvHD. Furthermore, stimulation of monocytes with S100 proteins was found to promote Th17 development, emphasizing the role of S100 proteins in Th17-triggered inflammation. Altogether, our results indicate that induction of Th17 cells by activated monocytes and the stimulatory effects of proinflammatory S100 proteins might play a relevant role in the pathogenesis of acute GvHD. Regarding our data, S100 proteins might be novel markers for the diagnosis and follow-up of GvHD.

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Comparison of 4 Neutrophil-Derived Proteins in Feces As Indicators of Disease Activity in Ulcerative Colitis

Abstract: Among the neutrophil-derived proteins in feces, PMN-e, Cal, and Lf represent useful markers of disease activity in patients with UC. Using all 3 markers in a composite index may be an additional noninvasive tool for the management of ambulant patients with UC.

Cited by 130 publications

References 34 publications

Matrix metalloproteinase-7 (matrilysin) controls neutrophil egress by generating chemokine gradients

Matrix metalloproteinase-7 (matrilysin) controls neutrophil egress by generating chemokine gradients

Age-related faecal calprotectin, lactoferrin and tumour M2-PK concentrations in healthy volunteers

Monocyte-Induced Development of Th17 Cells and the Release of S100 Proteins Are Involved in the Pathogenesis of Graft-versus-Host Disease

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