Ozone exposure induces neuroendocrine stress response, which causes
lymphopenia. It was hypothesized that
ozone-induced increases in stress
hormones will temporally follow changes in circulating granulocytes, monocytes- and lymphocyte subpopulations. The goal of this study was to chronicle the changes in circulating stress
hormones,
cytokines, and leukocyte trafficking during 4 h exposure to
ozone. Male Wistar Kyoto rats were exposed to air or
ozone (0.4 or 0.8 ppm) for 0.5, 1, 2, or 4 h. After each time point, circulating stress
hormones,
cytokines, and lung gene expression were assessed along with live and apoptotic granulocytes, monocytes (classical and non-classical), and lymphocytes (B, Th, and Tc) in blood, thymus, and spleen using flow cytometry. Circulating stress
hormones began to increase at 1 h of
ozone exposure. Lung expression of inflammatory
cytokines (Cxcl2,
Il6, and Hmox1) and
glucocorticoid-responsive genes (Nr3c1, Fkbp5 and Tsc22d3) increased in both a time- and
ozone concentration-dependent manner. Circulating granulocytes increased at 0.5 h of
ozone exposure but tended to decrease at 2 and 4 h, suggesting a rapid egress and then margination to the lung. Classical monocytes decreased over 4 h of exposure periods (∼80 % at 0.8 ppm). B and Tc lymphocytes significantly decreased after
ozone exposure at 2 and 4 h. Despite dynamic shifts in circulating immune cell populations, few differences were measured in serum
cytokines.
Ozone neither increased apoptotic cells nor altered thymus and spleen lymphocytes. The data show that
ozone-induced increases in adrenal-derived stress
hormones precede the dynamic migration of circulating immune cells, likely to the lung to mediate
inflammation.