Human macrophage immunometabolism regulator (MACIR) in patients with periodontitis

Immunobiology. 2023 Nov;228(6):152760. doi: 10.1016/j.imbio.2023.152760. Epub 2023 Nov 7.

Abstract

Objective: Periodontitis is a local inflammatory reaction caused by bacterial infection in which immune cells, including macrophages, are involved. Recent studies have shown that an important regulator of macrophage function is the human macrophage immunometabolism regulator (MACIR). This gene has been shown to play a key role in modulating the immune response by affecting the activity of fibroblasts and macrophages. In this study, we investigated the expression of MACIR in the gingival tissues of patients with periodontal disease, as well as the effect of IL-1β and TNF-α on the expression of MACIR gene and protein in human gingival fibroblasts.

Methods: MACIR mRNA expression in gingival tissue samples was determined using Real-time PCR. Expression of MACIR protein was determined using immunofluorescent staining and western blotting.

Results: The MACIR mRNA expression in gingival tissue samples in patients with periodontitis was statistically significantly lower than in gingival tissue samples from healthy controls (p = 0.009). The stimulation of human gingival fibroblasts with IL-1β and TNF-α resulted in a statistically significant decrease of MACIR gene mRNA expression. In western blotting and immunofluorescent analysis, we confirmed that the stimulation of the primary culture of human gingival fibroblasts by both IL-1β and TNF-α decreases the expression of MACIR protein.

Conclusion: The results of the study suggest that MACIR is an important regulator of the inflammatory process in patients with periodontitis. Decreased expression of the MACIR gene may activate macrophages to secrete mediators that increase inflammation and cause periodontal tissue destruction.

Keywords: Gene; Gingiva; MACIR; Periodontitis.

MeSH terms

  • Fibroblasts / metabolism
  • Gingiva
  • Humans
  • Inflammation / metabolism
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Macrophages / metabolism
  • Periodontitis*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Tumor Necrosis Factor-alpha* / genetics
  • Tumor Necrosis Factor-alpha* / metabolism

Substances

  • Tumor Necrosis Factor-alpha
  • Interleukin-1beta
  • RNA, Messenger