title: Modulation of neurological related allergic reaction in mice exposed to low-level toluene.
abstract: The contributing role of indoor air pollution to the development of allergic disease has become increasingly evident in public health problems. It has been reported that extensive communication exists between neurons and immune cells, and neurotrophins are molecules potentially responsible for regulating and controlling this neuroimmune crosstalk. The adverse effects of volatile organic compounds which are main indoor pollutants on induction or augmentation of neuroimmune interaction have not been fully characterized yet. To investigate the effects of low-level toluene inhalation on the airway inflammatory responses, male C3H mice were exposed to filtered air (control), 9 ppm, and 90 ppm toluene for 30 min by nose-only inhalation on Days 0, 1, 2, 7, 14, 21, and 28. Some groups of mice were injected with ovalbumin intraperitoneally before starting exposure schedule and these mice were then challenged with aerosolized ovalbumin as booster dose. For analysis of airway inflammation, bronchoalveolar lavage (BAL) fluid were collected to determine inflammatory cell influx and lung tissue and blood samples were collected to determine cytokine and neurotrophin mRNA and protein expressions and plasma antibody titers using real-time RT-PCR and ELISA methods respectively. Exposure of the ovalbumin-immunized mice to low-level toluene resulted in (1) increased inflammatory cells infiltration in BAL fluid; (2) increased IL-5 mRNA, decreased nerve growth factor receptor tropomyosin-related kinase A and brain-derived neurotrophic factor mRNAs in lung; and (3) increased IgE and IgG(1) antibodies and nerve growth factor content in the plasma. These findings suggest that low-level toluene exposure aggravates the airway inflammatory responses in ovalbumin-immunized mice by modulating neuroimmune crosstalk.
authors.affiliation: Research Center for Environmental Risk, National Institute for Environmental Studies 16-2, Onogawa, Tsukuba, Ibaraki 305-8506, Japan.
authors.lastname: Tin-Tin-Win-Shwe
authors.forename: Shoji
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Daisuke
authors.initials: D
authors.lastname: Nakajima
authors.forename: Akiko
authors.initials: A
authors.lastname: Furuyama
authors.forename: Atsushi
authors.initials: A
authors.lastname: Fukushima
authors.forename: Sohel
authors.initials: S
authors.lastname: Ahmed
authors.forename: Sumio
authors.initials: S
authors.lastname: Goto
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Fujimaki
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D003345:Corticosterone / Q000097:blood; D016207:Cytokines / Q000096:biosynthesis; D006967:Hypersensitivity / Q000473:pathology*; D007073:Immunoglobulin E / Q000096:biosynthesis; D007074:Immunoglobulin G / Q000096:biosynthesis; D008168:Lung / Q000378:metabolism; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D009414:Nerve Growth Factors / Q000096:biosynthesis; D020258:Neurotoxicity Syndromes / Q000473:pathology*; D010047:Ovalbumin / Q000276:immunology; D012333:RNA, Messenger / Q000096:biosynthesis; D020239:Receptor Cross-Talk / Q000276:immunology / Q000502:physiology; D017475:Receptors, Nerve Growth Factor / Q000096:biosynthesis; D012130:Respiratory Hypersensitivity / Q000473:pathology / Q000503:physiopathology; D012997:Solvents / Q000633:toxicity*; D014050:Toluene / Q000633:toxicity*
chemical_list: D016207:Cytokines; D007074:Immunoglobulin G; D009414:Nerve Growth Factors; D012333:RNA, Messenger; D017475:Receptors, Nerve Growth Factor; D012997:Solvents; D007073:Immunoglobulin E; D014050:Toluene; D010047:Ovalbumin; D003345:Corticosterone