Humoral immunity and regulation of intrapulmonary growth of Legionella pneumophila in the immunocompetent host

• Published in: The Journal of immunology (1950) Vol. 157; no. 11; pp. 5002 - 5008
• Main Authors: Brieland, JK, Heath, LA, Huffnagle, GB, Remick, DG, McClain, MS, Hurley, MC, Kunkel, RK, Fantone, JC, Engleberg, C
• Format: Journal Article
• Language: English
• Published: United States Am Assoc Immnol 01.12.1996
• Subjects: Animals; Antibodies, Bacterial - biosynthesis; Complement System Proteins - metabolism; Female; Immunocompetence; Legionella pneumophila; Legionella pneumophila - growth & development; Legionella pneumophila - immunology; Legionnaires' Disease - etiology; Legionnaires' Disease - immunology; Legionnaires' Disease - microbiology; Lung - immunology; Lung - microbiology; Macrophages, Alveolar - immunology; Mice; Mice, Inbred A; Opsonin Proteins - metabolism; Phagocytosis; Time Factors
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.157.11.5002

The potential role of humoral immunity in regulating intrapulmonary growth of Legionella pneumophila in the immunocompetent host was investigated using a murine model of Legionnaires' disease. Intratracheal inoculation of A/J mice with a virulent strain of L. pneumophila (10(6) bacteria per mouse) resulted in the recruitment of B lymphocytes into the lung and the development of anti-L. pneumophila Ab. Opsonization of L. pneumophila in vitro with anti-L. pneumophila-specific mAb resulted in a significant decrease in intrapulmonary growth of the bacteria at 24 to 72 h postinfection. Transmission electron microscopic analysis of lung tissue from L. pneumophila- infected mice demonstrated that while there was no significant difference between phagocytosis of the unopsonized and opsonized L. pneumophila by alveolar macrophages at 24 h postinfection, phagocytosis of opsonized bacteria by alveolar mononuclear phagocytic cells was significantly enhanced at 48 h postinfection. Depletion of A/J mice of complement before intratracheal inoculation of opsonized L. pneumophila (10(6) bacteria per mouse) did not significantly alter intrapulmonary growth of L. pneumophila. These results suggest that anti-L. pneumophila Ab, produced during replicative L. pneumophila lung infections, may regulate intrapulmonary growth of L. pneumophila in the immunocompetent host by decreasing the viability of extracellular L. pneumophila and by enhancing phagocytosis of the bacteria by alveolar mononuclear phagocytic cells by a complement-independent mechanism.