ArticleInfection and immunity1999
Invasion of human mucosal epithelial cells by Neisseria gonorrhoeae upregulates expression of intercellular adhesion molecule 1 (ICAM-1).
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- The bactericidal FabI inhibitor Debio 1453 clears antibiotic-resistant Neisseria gonorrhoeae infection in vivo.Nature communications · 2025Article
- Cyclization increases bactericidal activity of arginine-rich cationic cell-penetrating peptide forMicrobiology spectrum · 2024Article
- The association of host genes with specific sexually transmitted infections.Frontiers in reproductive health · 2023Review
- Three-dimensional models of the cervicovaginal epithelia to study host-microbiome interactions and sexually transmitted infections.Pathogens and disease · 2022Article
- Article
- Lactobacillus crispatus and its enolase and glutamine synthetase influence interactions between Neisseria gonorrhoeae and human epithelial cells.Journal of microbiology (Seoul, Korea) · 2020Article
- Exploitation ofFrontiers in immunology · 2019Review
- IL-36γ Augments Host Defense and Immune Responses in Human Female Reproductive Tract Epithelial Cells.Frontiers in microbiology · 2016Article
- Secretory leukocyte protease inhibitor binds to Neisseria gonorrhoeae outer membrane opacity protein and is bactericidal.American journal of reproductive immunology (New York, N.Y. : 1989) · 2012Article
- Late repression of NF-κB activity by invasive but not non-invasive meningococcal isolates is required to display apoptosis of epithelial cells.PLoS pathogens · 2011Article
- Neisseria gonorrhoeae infection protects human endocervical epithelial cells from apoptosis via expression of host antiapoptotic proteins.Infection and immunity · 2009Article
- Acinetobacter baumannii invades epithelial cells and outer membrane protein A mediates interactions with epithelial cells.BMC microbiology · 2008Article
- TREM-2 binds to lipooligosaccharides of Neisseria gonorrhoeae and is expressed on reproductive tract epithelial cells.Mucosal immunology · 2008Article
- Strain-specific differences in Neisseria gonorrhoeae associated with the phase variable gene repertoire.BMC microbiology · 2005Article
- Article
- Expression of proinflammatory cytokines and receptors by human fallopian tubes in organ culture following challenge with Neisseria gonorrhoeae.Infection and immunity · 2003Article
- Immortalization of human urethral epithelial cells: a model for the study of the pathogenesis of and the inflammatory cytokine response to Neisseria gonorrhoeae infection.Infection and immunity · 2002Article
- Distinct proinflammatory host responses to Neisseria gonorrhoeae infection in immortalized human cervical and vaginal epithelial cells.Infection and immunity · 2001Article
- Immunological basis for reactivation of tuberculosis in mice.Infection and immunity · 2001Article
- Endothelial adhesion molecule expression and its inhibition by recombinant bactericidal/permeability-increasing protein are influenced by the capsulation and lipooligosaccharide structure of Neisseria meningitidis.Infection and immunity · 1999Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Infection of the mucosa by Neisseria gonorrhoeae involves adherence to and invasion of epithelial cells. Little is known, however, about the expression by mucosal epithelial cells of molecules that mediate cellular interactions between epithelial cells and neutrophils at the site of gonococcal infection. The aim of this study was to determine the expression of intercellular adhesion molecule 1 (ICAM-1) by epithelial cells during the process of gonococcal invasion. The highly invasive strain FA1090 and the poorly invasive strain MS11 were incubated with human endometrial adenocarcinoma (HEC-1-B) or human cervical carcinoma (ME-180) epithelial cells, after which ICAM-1 expression was measured by flow cytometry. After 15 h of infection with FA1090, expression of ICAM-1 increased 4.7- and 2.1-fold for HEC-1-B and ME-180 cells, respectively, whereas 15 h of infection of HEC-1-B cells with MS11 increased ICAM-1 expression only 1.6-fold. ICAM-1 expression was restricted to the cell surface, since no soluble ICAM-1 was detected. The distribution of staining was heterogeneous and mimicked that seen after treatment of HEC-1-B cells with the ICAM-1 agonist tumor necrosis factor alpha (TNF-alpha) in the absence of bacteria. PCR and dot blot analyses of ICAM-1 mRNA showed no change in levels over time in response to infection. Although TNF-alpha was produced by HEC-1-B cells after infection, the extent of ICAM-1 upregulation was not affected by neutralizing anti-TNF-alpha antiserum. Dual-fluorescence flow cytometry showed that the cells with the highest levels of ICAM-1 expression were cells with associated gonococci. We conclude that epithelial cells upregulate the expression of ICAM-1 in response to infection with invasive gonococci. On the mucosa, upregulation of ICAM-1 by infected epithelial cells may function to maintain neutrophils at the site of infection, thereby reducing further invasion of the mucosa by gonococci.
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