Inhalation of diesel exhaust for three months affects major cytokine expression and induces bronchus-associated lymphoid tissue formation in murine lungs.

The authors investigated the effects of exposure to diesel exhaust (DE) on murine lung tissues in vivo. BALB/c and C57BL/6 mice were exposed to DE with low (100 microg/m(3)) and high (3 mg/m(3)) DE particle levels for 3 months. The authors then examined morphological changes and the expression of mRNAs for various cytokines (tumor necrosis factor [TNF]-alpha, interleukin [IL]-1beta, IL-4, IL-6, IL-10, IL-12p40, and interferon [IFN]-gamma) and inducible nitric oxide synthase (iNOS) in the lungs, as well as TNF-alpha, IL-1beta, IL-10, IL-12p40, and Mac-1 mRNA expression in alveolar macrophages (AMs). TNF-alpha, IL-12p40, IL-4, and IL-10 mRNA expression were mildly increased, whereas IL-1beta mRNA and iNOS expression were slightly decreased, in the low- and high-level exposure groups. Flow cytometry of bronchoalveolar lavage fluid revealed a significant increase in Mac-1-positive cells in the high-level exposure group. On histological examination, bronchus-associated lymphoid tissue (BALT), containing B and T lymphocytes, had developed only in the high-level exposure group. Chronic inhalation of DE influences cytokine expression in the murine lung, and induces phagocytosis and BALT development. These findings suggest that DE may provoke immunological responses by acting as a foreign body in the lung, and that even low-level exposure may induce allergic reactions.