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Peritoneal inflammation and fibrosis in C‐reactive protein transgenic mice undergoing peritoneal dialysis solution treatment
Author(s) -
Poon Peter YamKau,
Lan HuiYao,
Kwan Bonnie ChingHa,
Huang XiaoRu,
Chow KaiMing,
Szeto CheukChun,
Li Philip KamTao
Publication year - 2017
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/nep.12741
Subject(s) - medicine , peritoneal dialysis , fibrosis , inflammation , ctgf , peritoneum , tumor necrosis factor alpha , c reactive protein , peritonitis , genetically modified mouse , pathology , immunohistochemistry , creatinine , growth factor , transgene , chemistry , receptor , biochemistry , gene
Aim C‐reactive protein (CRP) is a mediator of systemic inflammation. Peritoneal dialysis (PD) is known to cause peritoneal inflammation and fibrosis. We compare the degree of peritoneal inflammation and fibrosis in wild‐type (WT) and CRP‐transgenic (Tg) mice after PD treatment. Methods WT ( n = 7) and CRP‐Tg ( n = 10) C57BL/6 J mice (all male, 10–12 weeks old) were injected intra‐peritoneally with 4.25% dextrose PD solution (3 mL/mouse) daily for 28 days, followed by a 2‐h peritoneal equilibration test (PET). The mice were then killed. Parietal peritoneal and omental tissues were collected for the assessment of inflammation and fibrosis. Results After 28 days of PD treatment, CRP‐Tg mice had higher dialysate‐to‐plasma (D/P) creatinine ratio than that of WT mice. Parietal peritoneum of the CRP‐Tg mice was more cellular and thicker than that of the WT mice. CRP‐Tg mice also had higher connective tissue growth factor (CTGF), intercellular adhesion molecule 1 (ICAM1) and tumor necrosis factor α (TNFα) RNA expressions as well as immunohistochemical staining in the parietal peritoneum than that of the WT mice. Conclusions CRP‐Tg mice have significantly more inflammation and fibrosis than WT mice after PD treatment. Our results suggest that CRP play a role in inflammation and fibrosis induced by PD. The implication of our results to human PD therapy needs further investigations.