R Nishino1, T Fukuyama, Y Tajima, L Miyashita, Y Watanabe, H Ueda, T Kosaka. 1. Laboratory of Immunotoxicology and Acute Toxicology, Toxicology Division, Institute of Environmental Toxicology, Uchimoriya-machi 4321, Joso-shi, Ibaraki 303-0043, Japan.
Abstract
BACKGROUND: Immunosuppressive environmental chemicals may increase the potency of allergens and thereby play a role in the development of respiratory tract allergies, such as allergic rhinitis and asthma. OBJECTIVES: We investigated the association between environmental immunosuppressive chemicals and the allergic airway inflammation development. METHODS: We used a mouse model of ovalbumin (OVA)-induced allergic airway inflammation. NC/Nga mice were exposed orally to pesticides parathion (an organophosphate compound) or methoxychlor (an organochlorine compound), or to an insecticide synergist piperonyl butoxide, prior to OVA intraperitoneal sensitization and inhalation challenge. We assessed serum IgE levels, B-cell counts, cytokine production, IgE production in hilar lymph nodes, eosinophil counts, chemokine levels in bronchoalveolar lavage fluid, and cytokine gene expression in the lung. RESULTS: Exposure to environmental immunosuppressive chemicals markedly increased serum IgE - IgE-positive B-cells, IgE and cytokines in lymph nodes - eosinophils and chemokines in BALF - IL-10a and IL-17 in the lung. CONCLUSIONS: Allergic airway inflammation can be aggravated by prior exposure to immunosuppressive environmental chemicals.
BACKGROUND: Immunosuppressive environmental chemicals may increase the potency of allergens and thereby play a role in the development of respiratory tract allergies, such as allergic rhinitis and asthma. OBJECTIVES: We investigated the association between environmental immunosuppressive chemicals and the allergic airway inflammation development. METHODS: We used a mouse model of ovalbumin (OVA)-induced allergic airway inflammation. NC/Nga mice were exposed orally to pesticides parathion (an organophosphate compound) or methoxychlor (an organochlorine compound), or to an insecticide synergist piperonyl butoxide, prior to OVA intraperitoneal sensitization and inhalation challenge. We assessed serum IgE levels, B-cell counts, cytokine production, IgE production in hilar lymph nodes, eosinophil counts, chemokine levels in bronchoalveolar lavage fluid, and cytokine gene expression in the lung. RESULTS: Exposure to environmental immunosuppressive chemicals markedly increased serum IgE - IgE-positive B-cells, IgE and cytokines in lymph nodes - eosinophils and chemokines in BALF - IL-10a and IL-17 in the lung. CONCLUSIONS:Allergic airway inflammation can be aggravated by prior exposure to immunosuppressive environmental chemicals.
Authors: Kannan Badri Narayanan; Manaf Ali; Barry J Barclay; Qiang Shawn Cheng; Leandro D'Abronzo; Rita Dornetshuber-Fleiss; Paramita M Ghosh; Michael J Gonzalez Guzman; Tae-Jin Lee; Po Sing Leung; Lin Li; Suidjit Luanpitpong; Edward Ratovitski; Yon Rojanasakul; Maria Fiammetta Romano; Simona Romano; Ranjeet K Sinha; Clement Yedjou; Fahd Al-Mulla; Rabeah Al-Temaimi; Amedeo Amedei; Dustin G Brown; Elizabeth P Ryan; Annamaria Colacci; Roslida A Hamid; Chiara Mondello; Jayadev Raju; Hosni K Salem; Jordan Woodrick; A Ivana Scovassi; Neetu Singh; Monica Vaccari; Rabindra Roy; Stefano Forte; Lorenzo Memeo; Seo Yun Kim; William H Bisson; Leroy Lowe; Hyun Ho Park Journal: Carcinogenesis Date: 2015-06 Impact factor: 4.944