Perinatal exposure to a representative
flame retardant, decabrominated
diphenyl ether (DBDE), was shown previously to increase viral titers in the lungs of respiratory syncytial virus (RSV)-infected offspring on day 5 post-
infection, resulting in exacerbation of
pneumonia. In this study, the significant increase of pulmonary viral titers was confirmed even on day 1 post-
infection and the effect on the primary immune response to
RSV infection were examined to assess a mode of DBDE action on developmental immunotoxicity. On day 1 after
infection, the secretion of both
TNF-alpha and
IL-6 decreased significantly in the bronchoalveolar lavage fluid prepared from RSV-infected offspring exposed to DBDE perinatally, but IL-1beta increased. However, in ex vivo
lipopolysaccharide stimulation test, the productivity of
TNF-alpha in the bronchoalveolar lavage cells, which are mainly primary immune cells responding to
RSV infection, prepared from offspring mice exposed to DBDE perinatally was not lower than that in the control. The primary immune cells retained normally the ability of
cytokine production after the DBDE exposure. Gene expressions of innate
pattern recognition receptors (
Toll-like receptor 3 and 4,
melanoma differentiation-associated gene-5, and
retinoic acid-inducible gene I) in lung tissues were not affected by DBDE exposure. Because the levels of
TNF-alpha,
IL-6, and IL-1beta are known to be elevated in the lungs of RSV-infected mice, these irregular productions due to perinatal DBDE exposure indicate a disorder of the primary immune response to
RSV infection. Thus, perinatal exposure to DBDE was suggested to cause a functional disorder of primary immunity responding to
RSV infection.