Up-regulated expression of costimulatory molecule CD80 on dendritic cells in mice with acute lung injury
10.3760/cma.j.issn.2095-4352.2016.06.012
- VernacularTitle:感染性急性肺损伤小鼠体内树突细胞 共刺激分子CD80表达呈上调趋势
- Author:
Jun LIU
;
Yunfu WU
;
Haibo QIU
- Publication Type:Journal Article
- Keywords:
Acute lung injury;
Dendritic cell;
Antigen;
CD80
- From:
Chinese Critical Care Medicine
2016;28(6):534-538
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the regularity of expression changes in CD80 in peripheral blood, lung and splenic dendritic cells (DCs) in mice with acute lung injury (ALI) induced by lipopolysaccharide (LPS) and its correlation with lung inflammation. Methods Twelve C57BL/6 mice were randomly divided into two groups, namely control group and ALI group, with 6 mice in each group. LPS (2 mg/kg) was intra-tracheal instilled in mice to reproduce ALI model, while the control mice received intra-tracheal administration of phosphate buffer saline (PBS) instead. The mice were sacrificed 6 hours after model reproduction, lung tissues were collected, and lung coefficient was calculated (lung wet weight/body weight ×100%). The pathological changes were examined under optical microscope after hematoxylin and eosin (HE) straining, the severity of lung injury was evaluated by the Smith score. Interleukin-6 (IL-6) level was determined by enzyme-linked immunosorbent assay (ELISA). After single-cell suspensions were isolated from the lung and spleen, the level of CD80 on DC in peripheral blood, lung and spleen was assessed by flow cytometry (FCM). The correlation between CD80 positive DC number and the severity of lung injury was analyzed by Spearman correlation method. Results Compared with control group, LPS-induced ALI resulted in a significant increase in lung coefficient [(0.67±0.04)% vs. (0.52±0.02)%, P < 0.05], and the levels of IL-6 were significantly enhanced (pg/mg: 2 712±475 vs. 335±168, P < 0.05). Histologically, widespread alveolar wall thickening caused by congested, severe hemorrhage in the interstitium and alveolus, and marked and diffuse interstitial infiltration with inflammatory cells were observed in ALI group. In contrast, no histological alteration was observed in the control group. In addition, the lung injury scores were markedly higher in ALI group than those in the control group (5.10±0.24 vs. 0.60±0.12, P < 0.05). It was shown by FCM analysis that there was a gradual but significant increase trend of CD80 positive dendritic cells number in blood, lung, and spleen in both control mice and ALI mice. However, no significant differences in the number of peripheral blood CD80 positive DCs were found between control group and ALI group [(3.3±1.5)% vs. (5.1±2.1)%, P > 0.05]. In contrast, there were a low but significantly higher percentage of CD80 positive DCs in the lung and spleen in ALI group than that in control group [Lung: (9.6±2.5)% vs. (3.6±1.2)%, spleen: (25.2±4.7)% vs. (9.0±3.6)%, both P < 0.05]. It was shown by the Spearman correlation analyses that respiratory CD80 positive DCs number was significantly positively correlated with IL-6 level in the lung (r = 0.761, P = 0.042) and the Smith score (r = 0.752, P = 0.047). Conclusions There is a significantly higher percentage of CD80 positive DCs in the lung and spleen in ALI mice, and a significantly positively correlation between respiratory CD80 positive DCs number and IL-6 level in the lung or the Smith score, which suggests elevated expression of CD80 on dendritic cells seems to play an important role in the pathogenesis of acute lung injury.
