Allergy-related cytokines (IL-4 and TNF-α) are induced by Di(2-ethylhexyl) phthalate and attenuated by plant-originated glycoprotein (75 kDa) in HMC-1 cells

Environ Toxicol. 2011 Aug;26(4):364-72. doi: 10.1002/tox.20563. Epub 2010 Jan 15.

Abstract

Phthalate esters as plasticizers have been widespread in the environment and may be associated with development of allergic diseases such as asthma and atopic dermatitis. In this study, we demonstrated that the CTB glycoprotein attenuates allergic reactions caused by di(2-ethylhexyl) phthalate (DEHP) in human mast cells (HMC-1). This experiment evaluated degranulation of histamine and β-hexosaminidase as well as activities of protein kinase C (PKC), stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), activator protein (AP)-1 and interleukin (IL)-4 and tumor necrosis factor (TNF)-α using immunoblotting and reverse transcription-polymerase chain reaction (RT-PCR). Our results revealed that the CTB glycoprotein in the presence of DEHP inhibits degranulation of mast cell, translocation of PKC from cytosol to membrane, and phosphorylation of SAPK/JNK in HMC -1 cells. We also found that the CTB glycoprotein (100 μg mL(-1) ) has suppressive effects on transcriptional activation of AP-1, and on the expression of IL-4 and TNF-α in DEHP-treated HMC-1 cells. We suggest that the CTB glycoprotein inhibits degranulation of mast cells and expressions of cytokines in HMC-1 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Allergic Agents / pharmacology*
  • Cell Line
  • Diethylhexyl Phthalate / toxicity*
  • Estrogens / toxicity*
  • Glycoproteins / pharmacology*
  • Histamine / metabolism
  • Humans
  • Hypersensitivity / drug therapy
  • Hypersensitivity / metabolism*
  • Interleukin-4 / antagonists & inhibitors
  • Interleukin-4 / genetics
  • Interleukin-4 / metabolism
  • JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Mast Cells
  • Moraceae / metabolism
  • Phosphorylation / drug effects
  • Plant Extracts / pharmacology
  • Plant Proteins / pharmacology*
  • Protein Kinase C / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transcription Factor AP-1 / metabolism
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • beta-N-Acetylhexosaminidases / antagonists & inhibitors
  • beta-N-Acetylhexosaminidases / metabolism

Substances

  • Anti-Allergic Agents
  • Estrogens
  • Glycoproteins
  • Plant Extracts
  • Plant Proteins
  • Transcription Factor AP-1
  • Tumor Necrosis Factor-alpha
  • Interleukin-4
  • Histamine
  • Diethylhexyl Phthalate
  • Protein Kinase C
  • JNK Mitogen-Activated Protein Kinases
  • beta-N-Acetylhexosaminidases