AB0080 IMBALANCE OF MONOCYTE/MACROPHAGE POLARIZATION IN PERIPHERAL BLOOD AND SYNOVIAL FLUID OF RHEUMATOID ARTHRITIS PATIENTS

医学 类风湿性关节炎 滑液 外周血 单核细胞 免疫学 病理 骨关节炎 替代医学
作者
Stefano Soldano,Emanuele Gotelli,P. Montagna,Rosanna Campitiello,Alberto Sulli,Vanessa Smith,Maurizio Cutolo
出处
期刊:Annals of the Rheumatic Diseases [BMJ]
卷期号:: 1218.2-1219
标识
DOI:10.1136/annrheumdis-2023-eular.5792
摘要

Background

Macrophages strongly contribute to the pathogenesis of rheumatoid arthritis (RA), initiating the inflammatory response, the join damage, but also may promote the resolution of inflammation and the restoration of tissue immune-homeostasis [1,2]. This seems to be related to an unbalanced immunological response mediated by macrophages through their polarization into "classically" and "alternatively" activated phenotypes (M1 or M2) [3,4]. However, little is known about the M1 and M2 phenotype of their circulating precursors (monocytes) in the peripheral blood (PB) and the synovial fluid (SF) of RA patients.

Objectives

To characterise the polarization status (M1 and M2) of PB and SF monocytes of RA patients together with their distribution in the monocyte subsets by flow cytometry (FC).

Methods

Nineteen RA patients not yet treated with biological DMARDs (mean age 62±14 years), who fulfilled the 2010 ACR/EULAR classification criteria for RA and treated in accordance with EULAR recommendation, as well as 19 age-matched healthy subjects (HSs) were enrolled after signed informed consent. PB and SF cells were collected from each RA patient, whereas only PB cells were collected from HSs. The expression of CD14 and CD16 surface markers allowed to identify the monocyte population and the monocyte subsets: "classical"(CD14++CD16-), "intermediate"(CD14++CD16+), and "non-classical"(CD14-CD16+). The M1 phenotype (M1 monocytes) was identified by the evaluation of CD80, CD86, TLR2 and TLR4, whereas the M2 phenotype (M2 monocytes) was identified evaluating CD204, CD163 and CD206 surface markers. Results were expressed as percentage of positive cells over total leukocytes from PB and SF. Statistical analysis was carried out by Mann-Whitney non-parametric test.

Results

In RA patients, the percentage of CD14++CD16+monocytes was significantly higher in PB compared to that in HS (p<0.001), and it was higher in SF compared to PB (p<0.05). The percentage of CD14-CD16+monocytes was significantly increased in RA-PB compared to HS-PB and RA-SF (p<0.01; p<0.05). RA patients were characterized by an increased percentage of M1 monocytes (CD80+CD86+TLR2+TLR4+CD204-CD163-CD206-cells) in PB compared to HSs and compared to RA-SF. The percentage of M2 monocytes (CD204+CD163+CD206+CD80-CD86-TLR2-TLR4-cells) was also increased in RA-PB compared to HS-PB and to RA-SF, but this increase was lower and not significant than that observed for M1 monocytes. Moreover, the M1-M2 monocyte ratio was 8:1in RA-PB. Therefore, in RA patients, circulating M1 monocytes belonged to the "non-classical" subset, whereas M2 monocytes belonged to the "classical" subset. The percentage of circulating mixed M1/M2 monocytes (CD80+CD86+TLR2+TLR4+CD204+CD163+CD206+cells) was higher in RA patients compared to HSs. Moreover, in RA patients, the percentage of these cells was higher in SF than in PB and they primarily belonged to the "intermediate" monocyte subset. Interestingly, the highest percentage of M2 and mixed M1/M2 monocytes was observed in PB and SF of RA patients receiving a higher daily (25mg) and cumulative glucocorticoid dosages.

Conclusion

The results confirm that RA is an immune-inflammatory disease mainly mediated by both M1 monocytes and macrophages, as demonstrated by the increase in the percentage of circulating M1 monocytes. Glucocorticoids might contribute to the M1 to M2 transition, which characterizes RA patients under remission by increasing mixed M1/M2 and M2 monocyte percentage.

References

[1]Okabe Y et al. Nat Immunol. 2016;17:9–17. [2]Kurowska-Stolarska M, et al. Nat Rev Rheumatol. 2022;18:384-97. [3]Cutolo M, et al. Front Immunol. 2022;13:867260. [4]Ross EA, et al. Front Immunol. 2021;12:708186.

Acknowledgements:

NIL.

Disclosure of Interests

Stefano Soldano: None declared, Emanuele Gotelli: None declared, Paola Montagna: None declared, Rosanna Campitiello: None declared, Alberto Sulli: None declared, Vanessa Smith: None declared, Maurizio Cutolo Grant/research support from: BMS, Boehringer, Amgen.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
安全123完成签到,获得积分20
1秒前
李嘉图的栗子完成签到,获得积分10
2秒前
Orange应助科研通管家采纳,获得10
2秒前
地表飞猪应助科研通管家采纳,获得10
2秒前
我是老大应助科研通管家采纳,获得10
2秒前
彭于晏应助chen采纳,获得10
2秒前
领导范儿应助科研通管家采纳,获得10
2秒前
汉堡包应助科研通管家采纳,获得10
2秒前
科研通AI2S应助科研通管家采纳,获得10
2秒前
斯文败类应助科研通管家采纳,获得10
2秒前
CipherSage应助科研通管家采纳,获得10
2秒前
隐形曼青应助科研通管家采纳,获得10
2秒前
SYLH应助科研通管家采纳,获得20
3秒前
3秒前
赘婿应助科研通管家采纳,获得10
3秒前
Owen应助科研通管家采纳,获得10
3秒前
田様应助科研通管家采纳,获得30
3秒前
JamesPei应助科研通管家采纳,获得10
3秒前
3秒前
所所应助科研通管家采纳,获得10
3秒前
昏睡的蟠桃应助科研通管家采纳,获得200
3秒前
搜集达人应助科研通管家采纳,获得10
3秒前
ding应助科研通管家采纳,获得10
3秒前
Jasper应助科研通管家采纳,获得10
4秒前
在水一方应助科研通管家采纳,获得10
4秒前
4秒前
Ava应助科研通管家采纳,获得10
4秒前
4秒前
4秒前
4秒前
4秒前
4秒前
4秒前
5秒前
5秒前
如云发布了新的文献求助10
6秒前
angela给angela的求助进行了留言
6秒前
6秒前
XZZH完成签到,获得积分10
7秒前
7秒前
高分求助中
【提示信息,请勿应助】关于scihub 10000
Les Mantodea de Guyane: Insecta, Polyneoptera [The Mantids of French Guiana] 3000
徐淮辽南地区新元古代叠层石及生物地层 3000
The Mother of All Tableaux: Order, Equivalence, and Geometry in the Large-scale Structure of Optimality Theory 3000
Global Eyelash Assessment scale (GEA) 1000
Picture Books with Same-sex Parented Families: Unintentional Censorship 550
Research on Disturbance Rejection Control Algorithm for Aerial Operation Robots 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 4038657
求助须知:如何正确求助?哪些是违规求助? 3576306
关于积分的说明 11375198
捐赠科研通 3306108
什么是DOI,文献DOI怎么找? 1819379
邀请新用户注册赠送积分活动 892698
科研通“疑难数据库(出版商)”最低求助积分说明 815066