E. Koike et al., Effect of exposure to nitrogen dioxide on alveolar macrophage-mediated immunosuppressive activity in rats, TOX LETT, 121(2), 2001, pp. 135-143
Nitrogen dioxide (NO2), a major component of air pollutants, induces inflam
matory responses in the lungs. Resident alveolar macrophages (AM) play an i
mmunosuppressive role in the lungs via suppression of lymphocyte proliferat
ion, and nitric oxide (NO) plays a crucial role in this immunosuppressive a
ctivity. Microenvironmental changes within the alveoli during inflammatory
responses, however, can inhibit this immunosuppressive activity of AM. The
present study was designed to clarify the effect of NO2 exposure on the imm
unosuppressive activity of and NO production by AM in rats, Wistar rats wer
e exposed to 10 ppm NO2 for 3, 14 or 28 days, after which bronchoalveolar l
avage fluid (BALF) was taken as a sample of the alveolar microenvironment.
Suppression of concanavalin A-induced lymphocyte proliferation and NO produ
ction by AM were markedly inhibited by BALF from NO2-exposed rats (NO2-BALF
), The inhibitory effect of NO2-BALF at 28-days exposure was stronger than
that of NO2-BALF at 3 or 14 days exposure. In conclusion, AM-mediated immun
osuppressive activity was inhibited by the NO2-induced changes of the alveo
lar microenvironment through the inhibition of NO production. (C) 2001 Else
vier Science Ireland Ltd. All rights reserved.