A. Erroi et al., IN-VIVO EXPOSURE TO NO2 REDUCES TNF AND IL-6 PRODUCTION BY ENDOTOXIN-STIMULATED ALVEOLAR MACROPHAGES, American journal of physiology. Lung cellular and molecular physiology, 15(1), 1996, pp. 132-138
Exposure to NO2 appears to affect lung defense mechanisms. We exposed
rats to 10 ppm of NO2 for 24 h or 7 days and studied the production of
tumor necrosis factor (TNF), interleukin-6 (IL-6), and prostaglandin
E(2) (PGE(2)) by alveolar macrophages after endotoxin stimulation. TNF
and IL-6 production was significantly decreased (four- to sixfold) in
the cell 13 sate of alveolar macrophages isolated from rats exposed t
o NO2. In parallel, PGE(2) production was significantly increased in t
he same samples and in the bronchoalveolar lavage fluid. Northern blot
analysis of the two cytokines indicated a reduction of the mRNA conte
nt. We also studied the expression of the TNF receptor type 1 (TNF-R1)
, known to neutralize TNF activity in its soluble form, and found that
expression of the mRNA was increased after endotoxin stimulation. We
can conclude that rats exposed to NO2 produce less TNF and IL-6 and th
at this might be related to increased PGE(2) production and increased
expression of TNF-R1.