Interleukin-32 positively regulates radiation-induced vascular inflammation.

Kobayashi H, Yazlovitskaya EM, Lin PC
Int J Radiat Oncol Biol Phys. 2009 74 (5): 1573-9

PMID: 19616744 · PMCID: PMC2713876 · DOI:10.1016/j.ijrobp.2009.04.017

PURPOSE - To study the role of interleukin-32 (IL-32), a novel protein only detected in human tissues, in ionizing radiation (IR)-induced vascular inflammation.

METHODS AND MATERIALS - Irradiated (0-6 Gy) human umbilical vein endothelial cells treated with or without various agents--a cytosolic phospholipase A2 (cPLA2) inhibitor, a cyclooxygenase-2 (Cox-2) inhibitor, or lysophosphatidylcholines (LPCs)--were used to assess IL-32 expression by Northern blot analysis and quantitative reverse transcriptase-polymerase chain reaction. Expression of cell adhesion molecules and leukocyte adhesion to endothelial cells using human acute monocytic leukemia cell line (THP-1) cells was also analyzed.

RESULTS - Ionizing radiation dramatically increased IL-32 expression in vascular endothelial cells through multiple pathways. Ionizing radiation induced IL-32 expression through nuclear factor kappaB activation, through induction of cPLA2 and LPC, as well as induction of Cox-2 and subsequent conversion of arachidonic acid to prostacyclin. Conversely, blocking nuclear factor kappaB, cPLA2, and Cox-2 activity impaired IR-induced IL-32 expression. Importantly, IL-32 significantly enhanced IR-induced expression of vascular cell adhesion molecules and leukocyte adhesion on endothelial cells.

CONCLUSION - This study identifies IL-32 as a positive regulator in IR-induced vascular inflammation, and neutralization of IL-32 may be beneficial in protecting from IR-induced inflammation.

MeSH Terms (13)

Cell Adhesion Molecules Cyclooxygenase 2 Cyclooxygenase 2 Inhibitors Endothelium, Vascular Group IV Phospholipases A2 Humans Interleukins NF-kappa B Subtilisins Umbilical Veins Vascular Cell Adhesion Molecule-1 Vascular Endothelial Growth Factor A Vasculitis

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