Association between perfluorooctanoic acid exposure and degranulation of mast cells in allergic inflammation.
Perfluorooctanoic acid (PFOA) has wide applications, including as a raw material for converted paper and packaging products. With the widespread use of PFOA, concerns regarding its potential environmental and health impacts have increased. In spite of the known hepatotoxicity and genotoxicity of PFOA, correlation with PFOA and allergic inflammation is not well known. In this study, the effect of PFOA on the degranulation of mast cells and mast cell-mediated allergic inflammation in the presence of FcεRI cross-linking was evaluated. In immunoglobulin (Ig) E-stimulated mast cells, PFOA increased the release of histamine and β-hexosaminidase by the up-regulation of intracellular calcium levels. PFOA enhanced gene expression of several pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8 by the activation of nuclear factor (NF)-κB in IgE-stimulated mast cells. Also, PFOA exacerbated allergic symptoms via hypothermia, and an increase of serum histamine, TNF-α, IgE and IgG1in the ovalbumin-induced systemic anaphylaxis. The present data indicate that PFOA aggravated FcɛRI-mediated mast cell degranulation and allergic symptoms. Copyright © 2016 John Wiley & Sons, Ltd.
CMRI, Departments of Pharmacology, Kyungpook National University, Daegu, Republic of Korea.
Jun-Kyoung
JK
Lee
CMRI, Departments of Pharmacology, Kyungpook National University, Daegu, Republic of Korea.|Natural Product Research Center, Research Institute of Bioscience and Biotechnology, Jeongeup, Republic of Korea.
Soyoung
S
Lee
Molecular Medicine, Kyungpook National University, Daegu, Republic of Korea.
Moon-Chang
MC
Baek
Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea.
Byung-Heon
BH
Lee
School of Life Science, Kyungpook National University, Daegu, Republic of Korea.
Hyun-Shik
HS
Lee
Department of Immunology, School of Medicine, Keimyung University, Daegu, Republic of Korea.
Taeg Kyu
TK
Kwon
College of Pharmacy, Yeungnam University, Gyeongsan, Republic of Korea.
Pil-Hoon
PH
Park
College of Pharmacy, Woosuk University, Jeonju, Republic of Korea.
Tae-Yong
TY
Shin
Department of Physiology, School of Medicine, Gachon University, Incheon, Republic of Korea.
Dongwoo
D
Khang
CMRI, Departments of Pharmacology, Kyungpook National University, Daegu, Republic of Korea.
Sang-Hyun
SH
Kim
D000707:Anaphylaxis / Q000139:chemically induced / Q000473:pathology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002210:Caprylates / Q000633:toxicity*; D015550:Cell Degranulation / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D016207:Cytokines / Q000096:biosynthesis; D005466:Fluorocarbons / Q000633:toxicity*; D006636:Histamine Release / Q000187:drug effects; D006967:Hypersensitivity / Q000473:pathology*; D007073:Immunoglobulin E / Q000276:immunology; D007141:Immunoglobulin Fc Fragments / Q000378:metabolism; D007249:Inflammation / Q000473:pathology*; D008297:Male; D008407:Mast Cells / Q000187:drug effects* / Q000473:pathology; D051379:Mice; D008813:Mice, Inbred ICR; D001619:beta-N-Acetylhexosaminidases / Q000378:metabolism
D002210:Caprylates; D016207:Cytokines; D005466:Fluorocarbons; D007141:Immunoglobulin Fc Fragments; D007073:Immunoglobulin E; C023036:perfluorooctanoic acid; D001619:beta-N-Acetylhexosaminidases; D002118:Calcium
allergic inflammation; histamine; mast cells; perfluorooctanoic acid (PFOA); pro-inflammatory cytokine