Usefulness of Monocytes/macrophages Activated With Low-dose Lipopolysaccharide in Tumor Tissue and Adipose Tissue of Obesity

Anticancer Res. 2019 Aug;39(8):4475-4478. doi: 10.21873/anticanres.13621.

Abstract

Chronic inflammation is involved in the development of cancer, lifestyle-related diseases, and autoimmune diseases. It also influences the severity of these diseases. Macrophages that accumulate in tumor tissues and adipose tissues of obesity have been shown to increase expression of inflammatory cytokines, thereby inducing inflammatory changes in these tissues. The macrophage phenotype is believed to be important in mediating inflammatory changes in tissues. Recently, monocytes/macrophages activated with low-dose lipopolysaccharide (LPS) were demonstrated to suppress increased expression of monocyte chemotactic protein (MCP)-1 and inflammatory cytokines (interleukin (IL)-1 β, IL-8, and tumor necrosis factor (TNF)-α). By suppressing the increased expression of chemotaxis-related and inflammation-related factors, monocytes/macrophages activated with low-dose LPS are considered to suppress the migration of macrophages into tissues and to regulate inflammatory changes in these tissues, respectively. The effects of macrophages activated with low-dose LPS were different from those of macrophages activated with high-dose LPS. In this review, we discuss the usefulness of monocytes/macrophages activation by low-dose LPS.

Keywords: Monocyte; adipocyte; cancer cell; low-dose lipopolysaccharide; macrophage; review.

Publication types

  • Review

MeSH terms

  • Adipose Tissue / metabolism
  • Adipose Tissue / pathology
  • Chemokine CCL2 / genetics
  • Dose-Response Relationship, Drug
  • Gene Expression Regulation / drug effects
  • Humans
  • Inflammation / drug therapy*
  • Inflammation / genetics
  • Interleukin-1beta / genetics
  • Interleukin-8 / genetics
  • Lipopolysaccharides / therapeutic use*
  • Macrophages / drug effects
  • Monocytes / drug effects
  • Neoplasms / drug therapy*
  • Neoplasms / genetics
  • Obesity / genetics*
  • Obesity / pathology
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • CCL2 protein, human
  • Chemokine CCL2
  • IL1B protein, human
  • Interleukin-1beta
  • Interleukin-8
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha