Gonorrhea: Epidemiology, Control and Prevention

Zenilman, Jonathan M.; Deal, Carolyn D.

doi:10.1016/b978-012663330-6/50017-6

Cited by 4 publications

(3 citation statements)

References 76 publications

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“…Our finding that endocervical epithelial cells can release higher levels of IL-1␣ in response to gonococcal infection than ectocervical and vaginal cells reveals an additional molecular mechanism for amplification of the proinflammatory responses which may contribute to the development of cervicitis, the most common clinical characteristic of the disease caused by N. gonorrhoeae in women (38). Moreover, other in vitro models have demonstrated that although macrophages upregulated a myriad of proinflammatory molecules following challenge with purified gonococcal antigens, they did not respond by significantly increased IL-1 production (24), suggesting that the endocervical epithelial cells may be the primary source of IL-1 during advanced stages of gonococcal disease.…”

Section: Discussionmentioning

confidence: 95%

“…A similar mechanism to control the bacterial colonization of the gastrointestinal mucosa has been proposed based on in vitro E. coli epithelial interactions (34). In contrast, the expression of CD66c by the endocervical epithelial cells upon infection can facilitate the gonococcal entry into the simple columnar epithelium of the endocervix, which is the primary site for gonococcal infection in the lower female genital tract (38).…”

Section: Discussionmentioning

confidence: 99%

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Distinct Proinflammatory Host Responses to Neisseria gonorrhoeae Infection in Immortalized Human Cervical and Vaginal Epithelial Cells

et al. 2001

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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.Cervicovaginal epithelial cells are increasingly recognized as active moderators of both innate and acquired immune functions in the genital tract via the production of a variety of proinflammatory and anti-inflammatory mediators. Increased levels of the cytokines interleukin 1 (IL-1), tumor necrosis factor alpha (TNF-␣), and IL-6 and the chemokines RANTES, MIP-1␣, and MIP-1␤ in cervicovaginal secretions have been associated with human immunodeficiency virus type 1 infection and bacterial vaginosis; however, little is known about the role of locally produced proinflammatory mediators in the pathogenesis of bacterial vaginitis and cervicitis (10). We recently developed three epithelial cell lines from normal human vagina, ectocervix, and endocervix, immortalized by expression of the E6 and E7 genes of human papillomavirus type 16 (8). The morphological and immunocytochemical characteristics of the immortalized lines closely resembled those of their tissues of origin and primary cultures, and all three differed significantly from the HeLa cervical adenocarcinoma cell line, the most commonly used cell line derived from the human female lower genital tract mucosa. The three cell lines constitutively produced distinctive arrays of cytokines (IL-1, IL-6, IL-7, macrophage colony-stimulating factor, and transforming growth factor ␤) and chemokines (IL-8 and RANTES),...

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Distinct Proinflammatory Host Responses to Neisseria gonorrhoeae Infection in Immortalized Human Cervical and Vaginal Epithelial Cells

et al. 2001

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“…The fact that GC has multiple strains and also has and the potential to cause some immunosuppression may result in a weak GC-specific immune response. Antibodies to GC in convalescing patients have not demonstrated protective immunity [42,43].…”

Section: Infection Control and Preventionmentioning

confidence: 99%

Extragenital manifestations of Neisseria gonorrhoeae

Spencer

Bash

2006

Curr Infect Dis Rep

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Neisseria gonorrhoeae is a common cause of genitourinary sexually transmitted infections. N. gonorrhoeae is an obligate human pathogen that has evidence of tissue-specific host interactions and diverse extragenital manifestations of infection both in adult and pediatric populations. The clinical presentation of extragenital gonorrhea, diagnostic methods, treatment and preventive measures are reviewed.

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