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Infection and Immunity, September 2001, p. 5840-5848, Vol. 69, No. 9
Fearing Research Laboratory, Department of
Obstetrics, Gynecology and Reproductive Biology, Brigham and Women's
Hospital, Harvard Medical School, Boston, Massachusetts
02115,1 and Section of Infectious
Diseases, Department of Medicine, Boston University School of Medicine,
Boston, Massachusetts 021182
Received 19 March 2001/Returned for modification 10 May
2001/Accepted 6 June 2001
In this study we utilized immortalized morphologically and
functionally distinct epithelial cell lines from normal human
endocervix, ectocervix, and vagina to characterize gonococcal
epithelial interactions pertinent to the lower female genital tract.
Piliated, but not nonpiliated, N. gonorrhoeae strain F62
variants actively invaded these epithelial cell lines, as demonstrated
by an antibiotic protection assay and confocal microscopy. Invasion of
these cells by green fluorescent protein-expressing gonococci was
characterized by colocalization of gonococci with F actin, which were
initially detected 30 min postinfection. In all three cell lines,
upregulation of interleukin 8 (IL-8) and IL-6, intercellular adhesion
molecule 1 (CD54), and the nonspecific cross-reacting antigen (CD66c)
were detected 4 h after infection with piliated and nonpiliated
gonococci. Furthermore, stimulation of all three cell lines with
gonococcal whole-cell lysates resulted in a similar upregulation of
IL-6 and IL-8, confirming that bacterial uptake is not essential for this response. Increased levels of IL-1 were first detected 8 h
after infection with gonococci, suggesting that the earlier IL-8 and
IL-6 responses were not mediated through the IL-1 signaling pathway.
The IL-1 response was limited to cultures infected with piliated
gonococci and was more vigorous in the endocervical epithelial cells.
The ability of gonococci to stimulate distinct proinflammatory host
responses in these morphologically and functionally different compartments of the lower female genital tract may contribute directly
to the inflammatory signs and symptoms characteristic of disease caused
by N. gonorrhoeae.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.9.5840-5848.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Distinct Proinflammatory Host Responses to Neisseria
gonorrhoeae Infection in Immortalized Human Cervical and
Vaginal Epithelial Cells
*
Corresponding author. Mailing address: Department of
Medicine, Section of Infectious Diseases, Boston University School of Medicine, 650 Albany St., Boston, MA 02118. Phone: (617) 414-5305. Fax:
(617) 414-5280. E-mail: caroline.genco{at}bmc.org.
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