HFD aggravated the arthritis and atherosclerosis by altering the intestinal status and gut microbiota

Mol Med. 2024 Dec 23;30(1):270. doi: 10.1186/s10020-024-01014-3.

Abstract

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.

Keywords: Arthritis combined with atherosclerosis; Gut microbiota; Inflammation; Intestinal status.

MeSH terms

  • Animals
  • Apolipoproteins E / deficiency
  • Apolipoproteins E / genetics
  • Apolipoproteins E / metabolism
  • Arthritis / etiology
  • Arthritis / microbiology
  • Atherosclerosis* / etiology
  • Atherosclerosis* / metabolism
  • Atherosclerosis* / microbiology
  • Atherosclerosis* / pathology
  • Diet, High-Fat* / adverse effects
  • Disease Models, Animal
  • Dysbiosis
  • Gastrointestinal Microbiome*
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / microbiology
  • Intestinal Mucosa / pathology
  • Intestines / microbiology
  • Intestines / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • T-Lymphocytes, Regulatory / immunology
  • T-Lymphocytes, Regulatory / metabolism
  • Th17 Cells / immunology
  • Th17 Cells / metabolism

Substances

  • Apolipoproteins E