HUMORAL IMMUNITY AND REGULATION OF INTRAPULMONARY GROWTH OF LEGIONELLA-PNEUMOPHILA IN THE IMMUNOCOMPETENT HOST

Citation
Jk. Brieland et al., HUMORAL IMMUNITY AND REGULATION OF INTRAPULMONARY GROWTH OF LEGIONELLA-PNEUMOPHILA IN THE IMMUNOCOMPETENT HOST, The Journal of immunology, 157(11), 1996, pp. 5002-5008
Citations number
48
Categorie Soggetti
Immunology
Journal title
The Journal of immunology
ISSN journal
00221767 → ACNP
Volume
157
Issue
11
Year of publication
1996
Pages
5002 - 5008
Database
ISI
SICI code
0022-1767(1996)157:11<5002:HIAROI>2.0.ZU;2-C
Abstract
The potential role of immunity in regulating intrapulmonary growth of Legionella pneumophila in the immunocompetent host was investigated us ing 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 lymphocytes: into the lung a nd the development of anti-L. pneumophila Ab. Opsonization of L. pneum ophila in vitro with anti-L. pneumophila-specific mAb resulted in a si gnificant decrease in intrapulmonary growth of the bacteria at 24 to 7 2 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 postinfe ction, phagocytosis of opsonized bacteria by alveolar mononuclear phag ocytic cells was significantly enhanced at 48 h postinfection. Depleti on of A/J mice of complement before intratracheal inoculation of opson ized L. pneumophila (10(6) bacteria per mouse) did not significantly a lter intrapulmonary growth of L. pneumophila. These results suggest th at anti-L, pneumophila Ab, produced during replicative L. pneumophila lung infections, may regulate intrapulmonary growth af L. pneumophila in the immunocompetent host by decreasing the viability of extracellul ar L. pneumophila and try enhancing phagocytosis of the bacteria by al veolar mononuclear phagocytic cells by a complement-independent mechan ism.