Cell-type-dependent induction of eotaxin and CCR3 by ionizing radiation

Biochem Biophys Res Commun. 2000 Mar 16;269(2):546-52. doi: 10.1006/bbrc.2000.2287.

Abstract

Eotaxin is an eosinophil-specific C-C chemokine that is implicated in the pathogenesis of eosinophilic inflammatory diseases, such as asthma and atopic dermatitis, by acting specifically on its receptor CCR3. Using RT-PCR analysis, we show that the expression of eotaxin is upregulated upon treatment with ionizing radiation (IR) in human dermal fibroblasts, but not in the bronchial epithelial cell line A549. In contrast, the gene encoding CCR3 is markedly induced in both cell types. None of the genes coding for other CCR3 ligands are significantly induced by IR in these cell types. cDNA array analysis of irradiated versus nonirradiated A549 cells and human dermal fibroblasts confirm and extend these results, and support the observation that regulation of eotaxin/CCR3-induction by IR occurs in a selective and cell-type-dependent manner. They further suggest that the induction of signaling via eotaxin and CCR3 may be an important step leading to eosinophilia in patients with radiation exposure.

MeSH terms

  • Base Sequence
  • Cell Line
  • Chemokine CCL11
  • Chemokines, CC*
  • Cytokines / biosynthesis*
  • Cytokines / genetics
  • DNA Primers
  • DNA, Complementary
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / radiation effects*
  • Humans
  • Interleukin-1 / pharmacology
  • RNA, Messenger / genetics
  • Radiation, Ionizing
  • Receptors, CCR3
  • Receptors, Chemokine / biosynthesis*
  • Receptors, Chemokine / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • CCL11 protein, human
  • CCR3 protein, human
  • Chemokine CCL11
  • Chemokines, CC
  • Cytokines
  • DNA Primers
  • DNA, Complementary
  • Interleukin-1
  • RNA, Messenger
  • Receptors, CCR3
  • Receptors, Chemokine
  • Tumor Necrosis Factor-alpha