The Effect of High-Fat Diet and Exercise Intervention on the TNF-α Level in Rat Spleen

Front Immunol. 2021 Dec 15:12:671167. doi: 10.3389/fimmu.2021.671167. eCollection 2021.

Abstract

High-fat diet (HFD) consumption can trigger chronic inflammation in some tissues. However, it remains unclear if HFD induces chronic inflammation in the spleen. This investigation aims to address the effect of HFD consumption and exercise intervention on the level of tumor necrosis factor alpha (TNF-α) in the spleen. Rats were subjected to HFD feeding and/or moderate-intensity treadmill running. The TNF-α levels in plasma and spleen were detected by ELISA. The mass and total cell numbers of the spleen were measured. In addition, the expression of TNF-α and its relevant gene mRNAs in macrophages from the spleen were analyzed by qRT-PCR. We found that HFD consumption did not significantly affect the mass and total cell numbers of the spleen. However, HFD consumption significantly increased splenic TNF-α level, the expression of TNF-α, toll-like receptor 4, and nuclear factor κB p65 mRNAs. In contrast, the expression of nicotinic acetylcholine receptor alpha 7 subunit (α7nAChR) mRNA in macrophages was downregulated. Additionally, exercise abolished the increase in splenic TNF-α level as well as the abnormal expression of TNF-α and related gene mRNAs in macrophages in HFD-fed rats. In conclusion, our results reveal that HFD consumption increases TNF-α level in the spleen, which is along with upregulation of the expression of TLR4 and NF-κB mRNAs as well as downregulation of the expression of α7nAChR mRNA in splenic macrophages in rats. Exercise abolished detrimental effects of HFD on TNF-α level in the spleen and prevented abnormal expression of these genes in the macrophages from rat spleen.

Keywords: exercise; high-fat diet; inflammation; spleen; tumor necrosis factor alpha.

MeSH terms

  • Animals
  • Diet, High-Fat / adverse effects*
  • Enzyme-Linked Immunosorbent Assay
  • Inflammation / etiology*
  • Inflammation / physiopathology
  • Inflammation / prevention & control
  • Macrophages / metabolism
  • Male
  • NF-kappa B / biosynthesis
  • NF-kappa B / genetics
  • Organ Specificity
  • Physical Conditioning, Animal*
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Running
  • Spleen / chemistry*
  • Toll-Like Receptor 4 / biosynthesis
  • Toll-Like Receptor 4 / genetics
  • Tumor Necrosis Factor-alpha / analysis*
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / genetics
  • alpha7 Nicotinic Acetylcholine Receptor / biosynthesis
  • alpha7 Nicotinic Acetylcholine Receptor / genetics

Substances

  • NF-kappa B
  • RNA, Messenger
  • Tlr4 protein, rat
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • alpha7 Nicotinic Acetylcholine Receptor