Complement and opsonins in alveolar secretions and serum of rats with pneumonia due to Streptococcus pneumoniae.

Complement appears to have an important role in the early defense against Streptococcus pneumoniae, but the role of complement as a defense mechanism within the lung is not well defined. Complement and heat-labile opsonins in pneumococcal pneumonia were studied by analysis of bronchoalveolar lavage fluid (BALF) of rats inoculated intratracheally with type 3 S. pneumoniae. BALF and serum were obtained at 0, 6, and 24 hr after infection. Leukocyte counts in BALF and histologic studies revealed an acute inflammatory response in the lung at 6 hr; this inflammation progressed for 24 hr. Levels of C1, C2, C3, and alternative pathway activity in pooled, concentrated (20X) BALF of normal and infected rats varied according to the stage of infection and the complement parameter studied, but in all cases the levels were only a small fraction of the levels in serum. Concentrated BALF had measurable levels of pneumococcal heat-labile opsonins, but these were also low as compared with serum levels. A small amount of C3 was detected by immunofluorescence on pneumococci recovered from BALF of infected animals, but these same organisms could be coated much more fully with C3 by brief incubation in serum. The milieu in the lung during bacterial infection is very different from that in serum and may be marginally suitable for effective opsonization of successful pulmonary pathogens such as type 3 S. pneumoniae.