There is increasing evidence that exposure to
air pollutants during pregnancy can result in a number of deleterious effects including low birth weight and the incidence of allergic
asthma. To investigate the in utero effects of DE exposure, timed pregnant BALB/c mice were exposed to 0, 0.8 or 3.1 mg/m(3) of DE during gestation days (GD) 9 to GD 18. The number of successful pregnancies was 15/20 in the air controls and 10/20 in each of the diesel exposures. Immune function in the 6-week-old offspring as determined by development of delayed type
hypersensitivity (DTH) reactions to
bovine serum albumin (BSA), antibody titers to injected sheep red blood cells (SRBC), splenic T cells expressing CD45(+)CD3(+)CD8(+) and CD3(+)CD25(+), and
mRNA expression of
TNF-alpha, TLR2, SP-A,
TGF-beta and Foxp3 in the lung were not affected by prenatal DE exposure. On the other hand, lung TLR4
mRNA expression, the number of neutrophils in the bronchoalveolar lavage fluid (BALF) and splenic T cells expressing CD45(+)CD3(+)CD4(+) and CD4(+)CD25(+) were differentially affected depending on the DE concentration and gender. When additional groups of mice were sensitized and challenged via the respiratory tract with
ovalbumin to induce allergic airway
inflammation, female mice had higher
protein levels in the BALF compared to males and this was reduced by prenatal exposure to either concentration of DE. No other changes in
allergen-induced immunity, lung function or severity of
inflammation were noted. Collectively, the results show that in utero exposure to DE altered some baseline inflammatory indices in the lung in a gender-specific manner, but had no effect on development of specific immune responses to experimental
antigens, or the severity of allergic
lung inflammation.