Interleukin-1 in obesity-related low-grade inflammation: From molecular mechanisms to therapeutic strategies

Int Immunopharmacol. 2021 Jul:96:107765. doi: 10.1016/j.intimp.2021.107765. Epub 2021 May 17.

Abstract

Since adipose tissue (AT) can upregulate pro-inflammatory interleukins (ILs) via storing extra lipids in obesity, obesity is considered the leading cause of chronic low-grade inflammation. These ILs can pave the way for the infiltration of immune cells into the AT, ultimately resulting in low-grade inflammation and dysregulation of adipocytes. IL-1, which is divided into two subclasses, i.e., IL-1α and IL-1β, is a critical pro-inflammatory factor. In obesity, IL-1α and IL-1β can promote insulin resistance via impairing the function of adipocytes and promoting inflammation. The current study aims to review the detailed molecular mechanisms and the roles of IL-1α and IL-1β and their antagonist, interleukin-1 receptor antagonist(IL-1Ra), in developing obesity-related inflammatory complications, i.e., type II diabetes (T2D), non-alcoholic steatohepatitis (NASH), atherosclerosis, and cognitive disorders. Besides, the current study discusses the recent advances in natural drugs, synthetic agents, and gene therapy approaches to treat obesity-related inflammatory complications via suppressing IL-1.

Keywords: Gene therapy; Inflammatory Diseases; Interleukin 1; Low-Grade Inflammation; Molecular Mechanism; Obesity.

Publication types

  • Review

MeSH terms

  • Adipose Tissue / immunology*
  • Adipose Tissue / pathology
  • Animals
  • Diabetes Mellitus, Type 2 / immunology
  • Diabetes Mellitus, Type 2 / pathology
  • Humans
  • Inflammation / drug therapy*
  • Inflammation / immunology
  • Inflammation / pathology
  • Interleukin-1 / antagonists & inhibitors*
  • Non-alcoholic Fatty Liver Disease / immunology
  • Non-alcoholic Fatty Liver Disease / pathology
  • Obesity / immunology*

Substances

  • Interleukin-1