Effect of lung damage by acute exposure to nitrogen dioxide on lung immunity in the rat

Exposure to nitrogen dioxide (NO₂) damages Type I alveolar epithelial cells and the epithelium of the terminal bronchiole. Because an intact epithelium may help control the number of inhaled particles that are cleared by the pulmonary lymphatics, damage to the alveolar epithelium could alter the antigen load to the lung-associated lymph nodes (LALN). To determine the effects of lung damage by NO₂ inhalation on lung immunity, we exposed adult, male rats to 26 ppm NO₂ for 24 hr at various time intervals before and after intratracheal immunization with 10⁸ sheep red blood cells (SRBC). Seven days after immunization, we determined the number of anti-SRBC antibody-forming cells (AFC) in the LALN, cervical lymph nodes, and spleen. The immunologic response to SRBC was limited to the LALN, with few or no AFC in either the cervical lymph nodes or spleen. A fivefold increase in the number of IgG anti-SRBC $\text{AFC}\text{10}{}^6$ LALN cells was evident in rats immunized 1 day after NO₂ exposure. The increase was followed by a slight suppression of the IgG response when rats were immunized 3 days after exposure, returning to normal levels by 7 days after exposure. Histopathological examination of lung tissues showed a slight respiratory bronchiolitis which was followed by a bronchiolar epithelial cell hyperplasia and Type II cell hyperplasia in the adjacent alveoli. Based on these observations, it appears that the fluctuations observed in the LALN response may be the result of damage and subsequent repair of bronchiolar and alveolar epithelium following NO₂ inhalation.