The mechanism of macrophage-inducible C-type lectin involved in uremic microinflammatory state
- VernacularTitle:巨噬细胞诱导型C型凝集素参与尿毒症微炎症状态及机制
- Author:
Lingshuang SUN
1
;
Meng WEI
1
;
Shanshan LIANG
1
;
Kehui SHI
1
;
Hongli JIANG
1
Author Information
- Publication Type:Journal Article
- Keywords: macrophage-inducible C-type lectin (Mincle); macrophage; microinflammation; uremia
- From: Journal of Xi'an Jiaotong University(Medical Sciences) 2023;44(4):525-531
- CountryChina
- Language:Chinese
- Abstract: 【Objective】 To explore the mechanism of macrophage-inducible C-type lectin (Mincle) and microinflammatory state in uremia. 【Methods】 SD rats were randomly divided into uremia group and sham operation group. The morphology and permeability of intestinal tissue, the morphology of intestinal tissue and macrophages were observed by transmission electron microscope, the expression of Mincle was detected in intestinal tissue sections, and the expressions of Toll-like receptor 4 (TLR-4) and NF-kappa B (NF-κB) protein on the surface of macrophages were detected by Western blotting. After the plasma was separated, the levels of endotoxin, C-reactive protein (CRP), interleulin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected by Limulus lysate dynamic turbidimetric assay, and enzyme-linked immunosorbent assay (ELISA). The data were analyzed with IBM SPSS19.0 software. 【Results】 The expression of Mincle in the jejunum, ileum, and colon in uremia group was higher than that in sham-operation group (P<0.05). The expressions of TLR4 and NF-κB protein significantly differed in the ileum, jejunum and colon in uremia group (P<0.001). The levels of endotoxin, CRP, IL-6, and TNF-α were significantly increased in uremia group compared with sham-operation group (P<0.05). 【Conclusion】 In uremia, Mincle on the surface of intestinal macrophages increases and further through TLR4/NF-κB pathway mediates the transformation of intestinal macrophages to M1 type, releasing inflammatory products and causing systemic microinflammation.
