© 2003 American Thoracic Society
Impaired Pulmonary Inflammatory Responses Are a Prominent Feature of Streptococcal Pneumonia in Mice with Experimental EmphysemaFirst Department of Internal Medicine, Yamagata University School of Medicine, Yamagata; Respiratory Medicine, Sei-rei Hamamatsu General Hospital, Shizuoka, Japan Correspondence and requests for reprints should be addressed to Sumito Inoue, M.D., First Department of Internal Medicine, Yamagata University School of Medicine, 2-2-2, Iida-Nishi, Yamagata 990-9585, Japan. E-mail: BYC04033{at}nifty.ne.jp
Little is known about why patients with chronic obstructive pulmonary disease are susceptible to bacterial infections. Using an animal model of pulmonary emphysema, we investigated the inflammatory responses to bacterial infection. After intratracheal infection with Streptococcus pneumoniae (103–107 cfu/mouse), the control mice did not die. However, the mice with emphysema died in a dose-dependent manner. Bronchoalveolar lavage fluid, examined 24 hours after infection showed that the numbers of total cells and neutrophils, in addition to murine tumor necrosis factor-
Key Words: chronic obstructive pulmonary disease • bacterial infection • cytokine • Streptococcus pneumoniae • bacteremia This article has been cited by other articles:
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and macrophage inflammatory protein-2 concentrations, were significantly less in the mice with emphysema compared with the control mice. Histopathologic findings revealed that the alveoli were filled with inflammatory cells and exudate in the control mice but not in the mice with emphysema. Seventy-two hours after infection, serum cytokine levels were significantly higher in the mice with emphysema, and significant numbers of S. pneumoniae were detected in both the whole lung tissues and the blood of mice with emphysema. These findings suggest that the inflammatory response in mice with emphysema was impaired at the site of bacterial infection despite the bacteremia, which accelerated severe systemic inflammatory responses. Accordingly, intra-alveolar but not systemic immune responses to bacterial infection were impaired in the presence of experimental emphysema. 
