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.