Mast Cell Infiltration Is Involved in Renal Interstitial Fibrosis in a Rat Model of Protein-Overload Nephropathy

Li, Ying; Zhou, Letiang; Liu, Fuyou; Peng, Youming; Li, Jun; Sun, Liang; Duan, Shao‐Bin; Ling, Guanghui; Chen, Xin; Jiang, Wen-ling; Xia, Yuncheng

doi:10.1159/000317102

Cited by 17 publications

(13 citation statements)

References 47 publications

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“…17 Moreover, mast cells have been reported to participate in the development of fibrosis. [10][11][12] Mast cells may promote fibrosis by inducing fibroblast proliferation, migration, contraction, and collagen production through the release of a range of stored cytokines such as TGF-β from mast cells that act in a paracrine fashion to stimulate fibroblasts. 18 Recently, it was shown that fibrosis in IgG4-related diseases is induced by cytokines (e.g.…”

Section: Discussionmentioning

confidence: 99%

Role of mast cells in fibrosis of classical Hodgkin lymphoma

Nakayama

Yokote

Hiraoka

et al. 2016

Int J Immunopathol Pharmacol

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The underlying mechanism of fibrosis in classical Hodgkin lymphoma (CHL) remains uncertain. This study aimed to investigate the association of fibrosis in the lymph nodes of patients with CHL through histological examination of the expression of cytokines associated with fibrosis and mast cell proliferation. Additionally, we sought to determine the degree of mast cell infiltration in a nodular sclerosis subtype of CHL (NSCHL) compared with that in non-NSCHL. We analyzed lymph nodes from 22 patients with CHL, of which eight were of the NSCHL and 14 of the non-NSCHL subtype, using immunohistochemical staining of forkhead box P3 (FOXP3), transforming growth factor (TGF)-β, interleukin (IL)-3, IL-13, and stem cell factor (SCF). Mast cells were positive for TGF-β and IL-13, and FOXP3-positive cells were negative for TGF-β. Only the expression of IL-13 in Hodgkin and Reed-Sternberg (HRS) cells was significantly more frequently observed in NSCHL than that in non-NSCHL (P = 0.0028) and was associated with a higher rate of fibrosis (P = 0.0097). The number of mast cells was significantly higher in NSCHL than that in non-NSCHL (P = 0.0001). A significantly positive correlation was observed between the rate of fibrosis and the number of mast cells (correlation coefficient, 0.8524; 95% CI, 0.6725-0.9372) (P <0.0001). The number of mast cells was significantly higher in the group with IL-13-positive HRS cells than that in the group with IL-13-negative HRS cells (P = 0.0157). Based on these findings, we hypothesize that IL-13 production by HRS cells may lead to fibrosis, and furthermore, promote mast cell proliferation and infiltration. This in turn might further produce the fibrotic cytokines IL-13 and TGF-β, resulting in fibrosis typical of NSCHL.

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Section: Discussionmentioning

confidence: 99%

Role of mast cells in fibrosis of classical Hodgkin lymphoma

Nakayama

Yokote

Hiraoka

et al. 2016

Int J Immunopathol Pharmacol

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“…Increased MC infiltration has been observed in various animal models of kidney fibrosis, including nephropathy induced by protein overload and the unilateral ureteral obstruction model . In a study conducted on MC‐competent vs MC‐deficient Ws/Ws rats, Miyazawa et al found that fibrosis occurring in conjunction with puromycin aminonucleoside‐nephrosis was not MC‐dependent.…”

Section: Mast Cells In Models Of Kidney Fibrosismentioning

confidence: 99%

The controversial role of mast cells in fibrosis

Bradding

Pejler

2018

Immunological Reviews

113

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Fibrosis is a medical condition characterized by an excessive deposition of extracellular matrix compounds such as collagen in tissues. Fibrotic lesions are present in many diseases and can affect all organs. The excessive extracellular matrix accumulation in these conditions can often have serious consequences and in many cases be life-threatening. A typical event seen in many fibrotic conditions is a profound accumulation of mast cells (MCs), suggesting that these cells can contribute to the pathology. Indeed, there is now substantialv evidence pointing to an important role of MCs in fibrotic disease. However, investigations from various clinical settings and different animal models have arrived at partly contradictory conclusions as to how MCs affect fibrosis, with many studies suggesting a detrimental role of MCs whereas others suggest that MCs can be protective. Here, we review the current knowledge of how MCs can affect fibrosis.

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“…[133–137], inversely correlating with renal function. [135, 137, 138] Mast cell deficiency has been associated with decreased fibrosis. [135] Mast cells have also been associated with antifibrotic actions.…”

Section: Cellular and Molecular Mediatorsmentioning

confidence: 99%