Expression of C-reactive protein in human lung epithelial cells and upregulation by cytokines and carbon particles

Inhal Toxicol. 2004 Aug;16(9):607-13. doi: 10.1080/08958370490464599.

Abstract

C-reactive protein (CRP) is the prototypic human acute-phase protein and is found at increased levels in the blood during episodes of inflammation. CRP was generally thought to be produced only by hepatocytes; however, several studies have shown extrahepatic synthesis of CRP. A previous study showed that PM10 and ultrafine carbon black (ufCB) were able to induce CRP expression in A549 cells. This study aims to examine the factors that lead to the production of CRP in A549 cells. A549 human lung epithelial cells were treated with cytokines (interleukin 6, tumor necrosis factor alpha, interferon gamma, or interleukin 1beta) or carbon particles (CB and ufCB) for 18 h. It was found that CRP could be expressed within the cells and that CRP was secreted from the cells particularly with tumor necrosis factor alpha, CB and ufCB treatments. It was also found that this expression of CRP with CB and ufCB treatments was dependent on nuclear factor kappa B (NFkappaB). The expression of CRP in A549 cells may indicate an important role for CRP expression and secretion from lung epithelial cells in response to inflammatory stimuli.

MeSH terms

  • Brefeldin A / pharmacology
  • C-Reactive Protein / metabolism*
  • Carbon / toxicity*
  • Cell Line, Tumor
  • Cytokines / pharmacology*
  • Enzyme-Linked Immunosorbent Assay
  • Epithelial Cells / metabolism
  • Fluorescent Antibody Technique
  • Humans
  • Lung / cytology
  • Lung / metabolism*
  • NF-kappa B / metabolism
  • Protein Synthesis Inhibitors / pharmacology
  • RNA, Messenger / biosynthesis
  • Reverse Transcriptase Polymerase Chain Reaction
  • Up-Regulation / physiology*

Substances

  • Cytokines
  • NF-kappa B
  • Protein Synthesis Inhibitors
  • RNA, Messenger
  • Brefeldin A
  • Carbon
  • C-Reactive Protein