ArticleClinical and experimental immunology2004
High-level endothelial E-selectin (CD62E) cell adhesion molecule expression by a lipopolysaccharide-deficient strain of Neisseria meningitidis despite poor activation of NF-kappaB transcription factor.
Article in Clinical and experimental immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Review
- Lentiviral MediatedFrontiers in immunology · 2022Article
- Local Anesthetic Ropivacaine Exhibits Therapeutic Effects in Cancers.Frontiers in oncology · 2022Review
- Colonization of dermal arterioles by Neisseria meningitidis provides a safe haven from neutrophils.Nature communications · 2021Article
- Comprehensive phenotyping of endothelial cells using flow cytometry 2: Human.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2021Review
- 7-Ketocholesterol enhances leukocyte adhesion to endothelial cells via p38MAPK pathway.PloS one · 2018Article
- Rationale for Adjunctive Therapies for Pediatric Sepsis Induced Multiple Organ Failure.Pediatric clinics of North America · 2017Review
- A critical role for ATF2 transcription factor in the regulation of E-selectin expression in response to non-endotoxin components of Neisseria meningitidis.Cellular microbiology · 2016Article
- Vascular endothelial injury and apoptosis in rats with severe acute pancreatitis.Gastroenterology research and practice · 2015Article
- Circulating endothelial cells in oncology: pitfalls and promises.British journal of cancer · 2008Review
- Gene expression pattern in human brain endothelial cells in response to Neisseria meningitidis.Infection and immunity · 2007Article
- MyD88-dependent signaling affects the development of meningococcal sepsis by nonlipooligosaccharide ligands.Infection and immunity · 2006Article
- Endotoxin immunity and the development of the systemic inflammatory response syndrome in critically ill children.Intensive care medicine · 2006Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Binding of host inflammatory cells to the endothelium is a critical contributor to the vascular damage characteristic of severe meningococcal disease and is regulated by endothelial cell adhesion molecules such as ICAM-1, VCAM-1 and CD62E. Intact meningococci induce far higher levels of CD62E than lipopolysaccharide (LPS) alone, whereas LPS is at least as potent as meningococci at inducing both VCAM-1 and ICAM-1 expression. This suggests that meningococci possess additional factors other than LPS present in whole bacteria that result in differential adhesion molecule expression. To investigate this possibility, we studied the capacity of an LPS-deficient isogenic strain of serogroup B Neisseria meningitidis H44/76 (lpxA-) to induce endothelial cell adhesion molecule expression and translocation of the transcription factor NF-kappaB, and compared it to both parent and unencapsulated strains of both B1940 and H44/76 and purified LPS. Although the LPS-deficient isogenic mutant of strain H44/76 was found to be a poor inducer of NF-kappaB, it induced higher levels of CD62E expression than LPS alone. These data provide evidence that intact meningococci induce a range of signals in the endothelium that are distinct from those seen with purified LPS alone and that they occur in a LPS-dependent and LPS-independent manner. These signals may explain the potent effects of N. meningitidis on CD62E expression on vascular endothelium and provide a basis for the complex endothelial dysregulation seen in meningococcal sepsis.
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