Characterization of the pulmonary inflammatory response to an anaerobic bacterial challenge

Anaerobic bacteria from the oral flora are important causes of aspiration pneumonia and lung abscess. However, the pulmonary antibacterial response to these organisms has not been well described. To define this, mice were intratracheally inoculated with 10⁹ Bacteroides gingivalis, a member of the B. melaninogenicus group, and a common clinical isolate from periodontal disease and anaerobic pulmonary infections. Studies after intratracheal challenge included bacteriologic and histopathologic examination, pulmonary cellular response, lactic dehydrogenase (LDH) and albumin levels in lung lavage fluid, and wet lung weight. Overall mortality was 25%. In the surviving animals, pulmonary lavage showed a marked recruitment of polymorphonuclear leukocytes that was associated with significant bacterial killing by 48 h. Histopathologic examination showed an acute, severe necrotizing bronchopneumonia. Pulmonary abscess formation occurred in 37% of animals. Severe parenchymal damage was further documented by a marked increase in LDH levels in lavage fluids. Mean LDH levels in lavage fluid increased to 850 ± 25 units/first lavage at 24 h postchallenge compared with control values of 65 ± 10 units/first lavage. Lung lavage also demonstrated an extensive influx of serum albumin consistent with injury to the alveolar capillary membrane. Albumin levels in lung lavage were highest at 24 h after intratracheal challenge (3.25 ± 0.3 mg/first lavage), whereas lavage fluid from control mice had non detectable albumin levels. Wet lung weights maximally increased from 0.12 ± 0.01 g in control mice to 0.28 ± 0.03 g 24 h after bacterial challenge. These data demonstrate that B. gingivalis causes marked inflammation in the lung that progresses to severe bronchopneumonia and lung abscess. This experimental model characterizes the normal pulmonary host responses against an anaerobic bacterium and can be further used to examine pulmonary-bacterial interactions in the pathogenesis of anaerobic lung infections.