Peritoneal Mast Cells in Peritoneal Dialysis Patients, Particularly in Encapsulating Peritoneal Sclerosis Patients

Alscher, Mark Dominik; Braun, Niko; Biegger, Dagmar; Fritz, Péter

doi:10.1053/j.ajkd.2006.11.040

Cited by 37 publications

(28 citation statements)

References 33 publications

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“…Although MCs can be found in biopsies of the parietal peritoneum of humans (Jimenez-Heffernan et al, 2006), and the number of MCs in these biopsies are markedly increased in inflammatory conditions, i.e. chronic appendicitis (Alscher et al, 2007), it is unclear whether these MCs within the peritoneal tissue can mediate the same protective effects as mouse peritoneal MCs in the peritoneal cavity. Skin MCs from mice and humans on the other hand share many characteristic features (Table 1), e.g.…”

Section: Resultsmentioning

confidence: 99%

Mast cell functions in the innate skin immune system

Metz¹,

Siebenhaar²,

Maurer³

2008

Immunobiology

107

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Section: Resultsmentioning

confidence: 99%

Mast cell functions in the innate skin immune system

Metz¹,

Siebenhaar²,

Maurer³

2008

Immunobiology

107

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“…In healthy peritoneum, mast cells are present and the number of mast cells increases upon infection [34,35] . Activated mast cells can induce new vessel formation by producing proangiogenic factors like TGF-␤ , basic fibroblast growth factor, VEGF, TNF-␣ and IL-8 (see above) [36,37] .…”

Section: Peritoneal Cells Involved In Pd-induced Angiogenesismentioning

confidence: 99%

Angiogenesis in Peritoneal Dialysis

Stavenuiter¹,

Schilte²,

Wee

et al. 2011

Kidney Blood Press Res

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Long-term exposure to peritoneal dialysis fluid induces morphological alterations, including angiogenesis, leading to a loss of ultrafiltration (UF) capacity. We discuss the effect of different factors in peritoneal dialysis (PD) on angiogenesis. In addition, we describe the process of angiogenesis and the possible role of different cell types in the peritoneum upon PD contributing to new blood vessel formation. Furthermore, we review several interventions used in our rat PD exposure model to decrease angiogenesis in PD. Moreover, we show new data on the use of sunitinib to inhibit angiogenesis in this rat model. Although various interventions seem to be promising, well-randomised clinical trials showing absolute prevention of angiogenesis and UF failure are, yet, still missing. To make real progress in PD treatment, the aim should be to prevent angiogenesis as well as peritoneal fibrosis and PD-induced inflammation.

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“…Contributing to the potential mechanism of EPS is a further finding we have recently studied in the peritoneal mast cells (MC) [19]: there is evidence for MC degranulation in all altered peritoneal tissues compared with the unstressed normal peritoneum. Mast cells contain stores and secrete – if stressed or activated by different receptor and nonreceptor-triggered pathways – many molecules, such as MC tryptase, chymase, basic fibroblast growth factor (bFGF), histamine, c-Kit oncoprotein and vascular endothelial growth factor (VEGF) [20,21,22,23,24].…”

Section: Discussionmentioning

confidence: 99%

Fibrogenic Growth Factors in Encapsulating Peritoneal Sclerosis

et al. 2009

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Background: Increased local levels of fibrogenic growth hormones contribute substantially to the process of encapsulating peritoneal sclerosis (EPS) in animal models. Methods: We analyzed probes from patients with normal kidney function (n = 10), with normal kidney function and inflammation (n = 10), on PD without (n = 10) and with EPS (n = 9). We investigated the degree of fibrosis and the number of vessels and vasculopathy. Additionally, we investigated the expression of NFκB, TGFβ1, TGFβ1 receptor, TGFβ2, TGFβ2 receptor, FGF-BP, CTGF and VEGF by immunohistochemistry. Results: In EPS, we found an exclusive upregulation of VEGF (normal 0, appendicitis 1.0 ± 1.2, PD 1.7 ± 1.8 and EPS 5.7 ± 4.4; p < 0.0001), whereas in PD, CTGF was significantly increased (normal 6.0 ± 2.8, appendicitis 7.3 ± 2.5, PD 10.0 ± 1.8 and EPS 7.3 ± 2.1; p = 0.0059). The results for the TGFβ system and NFκB were not uniform, in EPS no increases were demonstrable. Vasculopathy was significantly more pronounced in EPS (normal 0.4 ± 0.5, appendicitis 0.2 ± 0.3, PD 1.0 ± 0.7 and EPS 1.6 ± 1.2; p < 0.0001) than in PD or inflammation (normal 30 ± 16, appendicitis 82 ± 48, PD 1,936 ± 952 and EPS 2,613 ± 1,209; p < 0.0001), whereas the density of vessels were decreased (normal 125 ± 114, appendicitis 817 ± 347, PD 81 ± 57 and EPS 36 ± 33; p < 0.0001). Conclusions: The process of EPS was associated with increased VEGF in the peritoneum. The reduced density of vessels compared with marked fibrosis could point to hypoxia as an inducer.

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Peritoneal Mast Cells in Peritoneal Dialysis Patients, Particularly in Encapsulating Peritoneal Sclerosis Patients

Cited by 37 publications

References 33 publications

Mast cell functions in the innate skin immune system

Mast cell functions in the innate skin immune system

Angiogenesis in Peritoneal Dialysis

Fibrogenic Growth Factors in Encapsulating Peritoneal Sclerosis

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