Affiliation:
1. Channing Laboratory
2. Division of Infectious Diseases, Department of Medicine
3. Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115
Abstract
ABSTRACT
The adherence to and invasion of the human epithelial cell line A549 by group B streptococcus (GBS) serotype VIII strains were compared with those of serotype III strains by a conventional method and the dynamic in vitro attachment and invasion system. Twenty GBS strains, including nine vaginal isolates and one invasive isolate each of serotypes III and VIII, were used in the conventional attachment and invasion assay. Adherence to and invasion of A549 cells by serotype VIII GBS strains were significantly greater (
P
< 0.0001) than those by serotype III strains for both the invasive strain and vaginal isolates. Cytokine production by A549 cells following stimulation with GBS serotypes III and VIII or their purified capsular polysaccharides (CPS) was measured. Serotype III strains stimulated significantly greater tumor necrosis factor alpha (TNF-α) (
P
< 0.0001) and interleukin-10 (IL-10) (
P
< 0.05) production than did serotype VIII strains. IL-8 production in response to serotype VIII was significantly higher (
P
< 0.001) than that in response to serotype III. TNF-α, IL-8, and IL-10 production was greater in A549 cells infected with GBS than in the untreated control cells. TNF-α production was significantly greater (
P
< 0.005) after stimulation with purified GBS serotype III CPS than after stimulation with serotype VIII CPS, a result similar to that after stimulation with whole GBS. IL-12 production by A549 cells was observed only in response to infection with GBS serotype III, resulting in the possibility of a greater TH1 response in serotype III GBS. These results suggest differences in immune responses to infection with GBS serotypes III and VIII.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Reference50 articles.
1. Bogdan, C., Y. Vodovotz, and C. Nathan. 1991. Macrophage deactivation by interleukin-10. J. Exp. Med.174:1549-1555.
2. Campbell, J. R., S. L. Hillier, M. A. Krohn, P. Ferrieri, D. F. Zaleznik, and C. J. Baker. 2000. Group B streptococcal colonization and serotype-specific immunity in pregnant women at delivery. Obstet. Gynecol.96:498-503.
3. Cassatella, M. A., L. Meda, S. Bonora, M. Ceska, and G. Coinstantin. 1993. Interleukin 10 (IL-10) inhibits the release of proinflammatory cytokines from human polymorphonuclear leukocytes. Evidence for an autocrine role of tumor necrosis factor and IL-1 beta in mediating the production of IL-8 triggered by lipopolysaccharide. J. Exp. Med.178:2207-2211.
4. Davies, H. D., C. Adair, A. McGeer, M. Doreen, S. Robertson, M. Mucenski, L. Kowalsky, G. Tyrell, and C. J. Baker. 2001. Antibodies to capsular polysaccharide of group B Streptococcus in pregnant Canadian women: relationship to colonization status and infection in the neonate. J. Infect. Dis.184:285-291.
5. Detmers, P. A., S. K. Lo, E. Olsen-Egbert, A. Walz, M. Baggiolini, and Z. A. Cohn. 1990. Neutrophil-activating protein 1/interleukin-8 stimulates the binding activity of the leukocyte adhesion receptor XD11b/CD18 on human neutrophils. J. Exp. Med.171:1155-1162.
Cited by
24 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献