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BioMed Research International
Volume 2013 (2013), Article ID 151807, 7 pages
http://dx.doi.org/10.1155/2013/151807
Research Article

Perinatal Exposure to Insecticide Methamidophos Suppressed Production of Proinflammatory Cytokines Responding to Virus Infection in Lung Tissues in Mice

1Department of Microbiology, Graduate School of Clinical Pharmacy, Kyushu University of Health and Welfare, Yoshino 1714-1, Nobeoka, Miyazaki 882-8508, Japan
2Department of Biochemistry, Graduate School of Clinical Pharmacy, Kyushu University of Health and Welfare, Yoshino 1714-1, Nobeoka, Miyazaki 882-8508, Japan
3Division of Risk Assessment, Biological Safety Research Center, National Institute of Health Sciences, 1-18-1, Kamiyoga, Setagaya-ku, Tokyo 158-8501, Japan
4Department of Microbiology and Infectious Diseases, School of Pharmaceutical Sciences, Kyushu University of Health and Welfare, Yoshino 1714-1, Nobeoka, Miyazaki 882-8508, Japan

Received 1 May 2013; Revised 7 August 2013; Accepted 23 August 2013

Academic Editor: Edineia Lemos de Andrade

Copyright © 2013 Wataru Watanabe et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Methamidophos, a representative organophosphate insecticide, is regulated because of its severe neurotoxicity, but it is suspected of contaminating agricultural foods in many countries due to illicit use. To reveal unknown effects of methamidophos on human health, we evaluated the developmental immunotoxicity of methamidophos using a respiratory syncytial virus (RSV) infection mouse model. Pregnant mice were exposed to methamidophos (10 or 20 ppm) in their drinking water from gestation day 10 to weaning on postnatal day 21. Offsprings born to these dams were intranasally infected with RSV. The levels of interleukin-6 (IL-6) and interferon-gamma in the bronchoalveolar lavage fluids after infection were significantly decreased in offspring mice exposed to methamidophos. Treatment with methamidophos did not affect the pulmonary viral titers but suppressed moderately the inflammation of lung tissues of RSV-infected offspring, histopathologically. DNA microarray analysis revealed that gene expression of the cytokines in the lungs of offspring mice exposed to 20 ppm of methamidophos was apparently suppressed compared with the control. Methamidophos did not suppress IL-6 production in RSV-infected J774.1 cell cultures. Thus, exposure of the mother to methamidophos during pregnancy and nursing was suggested to cause an irregular immune response in the lung tissues in the offspring mice.