Shi Na, Jiang Shan, Zhao Yue, Zhang Yang, Duan Xinwang, Hong Guo-Bao, Yang Zhongshan, Duan Yuanyuan, Niu Haitao
Key Laboratory of Viral Pathogenesis and Infection Prevention and Control (Jinan University), Ministry of Education, School of Medicine, Jinan University, Guangzhou, 510632, China.
Guangzhou Key Laboratory for Germ-Free Animals and Microbiota Application, School of Medicine, Institute of Laboratory Animal Sciences, Jinan University, Guangzhou, 510632, China.
Mol Med. 2024 Dec 23;30(1):270. doi: 10.1186/s10020-024-01014-3.
Rheumatoid arthritis (RA) and cardiovascular disease (CVD) are both the chronic inflammatory disease. To investigate the influence of secondary atherosclerosis on arthritis mice, we treated the ApoE mice with K/BxN serum and high fat diet (HFD), and subsequently assessed the phenotypes as well as immune profiles of K/BxN serum and HFD induced ApoE mice. We found that HFD treatment aggravated the hyperlipidemia, atherosclerotic lesions, ankle swelling and arthropathy of mice. We further demonstrated that HFD altered the gut microbiota and metabolism, intestinal homeostasis and Th17/Treg cell balance in lamina propria lymphocytes. Moreover, HFD decreased the number of Peyer' s patches and altered the expression profiling of gut immune cells. In addition, HFD increased the number of aortic leukocytes and macrophages, then aggravated the atherosclerosis in aorta, which led to greater inflammation in mice aorta and aortic root. Collectively, our study indicated that HFD aggravated the arthritis and atherosclerosis, which may be contributed by microbiota dysbiosis, the intestinal permeability and disrupted immunological homeostasis.
类风湿性关节炎(RA)和心血管疾病(CVD)都是慢性炎症性疾病。为了研究继发性动脉粥样硬化对关节炎小鼠的影响,我们用K/BxN血清和高脂饮食(HFD)处理载脂蛋白E(ApoE)小鼠,随后评估K/BxN血清和HFD诱导的ApoE小鼠的表型以及免疫特征。我们发现,HFD处理加重了小鼠的高脂血症、动脉粥样硬化病变、踝关节肿胀和关节病。我们进一步证明,HFD改变了肠道微生物群和代谢、肠道稳态以及固有层淋巴细胞中的Th17/Treg细胞平衡。此外,HFD减少了派尔集合淋巴结的数量,并改变了肠道免疫细胞的表达谱。此外,HFD增加了主动脉白细胞和巨噬细胞的数量,进而加重了主动脉的动脉粥样硬化,导致小鼠主动脉和主动脉根部出现更严重的炎症。总的来说,我们的研究表明,HFD加重了关节炎和动脉粥样硬化,这可能是由微生物群失调、肠道通透性和免疫稳态破坏所致。