Thymus and pulmonary lymph node response to acute and subchronic ozone inhalation in the mouse.

Ozone is an oxidant gas which primarily injures the centroacinar portion of the lung. While the classical lesion of oxidant-mediated lung damage is relatively well described, the effect of this form of injury on the lymphocytic arm of the pulmonary defense system is less clear. In the present experiments we exposed CD-1 female mice to ozone at a level of 0.7 ppm for 20 hr per day for 1-28 days and observed the lymphocyte response in the pulmonary lymph nodes and the thymus. In the mediastinal lymph nodes we observed a marked hyperplastic response that was prominent in the paracortex and was characterized by the presence of blastic forms. In contrast, the thymus underwent an atrophic response characterized by cellular loss in the cortical region. Prior surgical adrenalectomy of ozone-exposed animals eliminated part, but not all of the thymic atrophy response, indicating that adrenal-mediated stress alone did not account for all of the observed effect. Thymectomy of animals prior to ozone exposure produced a 40% reduction in the mediastinal lymph node response, suggesting that a part of the node hyperplasia is thymus dependent. The results of these experiments indicate that lymphoid organs are altered following oxidant-mediated lung damage in the mouse. The changes are observed in the absence of exogenous antigenic stimulation and suggest that lymphoid cells are an integral aspect of the host response to high-level ozone inhalation.