Neisseria meningitidis colonizes the human nasopharynx and occasionally causes lethal or damaging septicemia and meningitis. Here, we examined the adherence-mediated signaling of meningococci to human cells by comparing gene expression profiles of human umbilical vein endothelial cells (HUVEC) infected by adherent wild-type, frpC-deficient mutant, or the nonadherent (DeltapilD) N. meningitidis. Pili-mediated adhesion of meningococci resulted in alterations of expression levels of human genes known to regulate apoptosis, cell proliferation, inflammatory response, adhesion and genes for signaling pathway proteins such as TGF-beta/Smad, Wnt/beta-catenin and Notch/Jagged. This reveals that adhering piliated meningocci manipulate host signaling pathways controlling cell proliferation while establishing a commensal relationship.
- MeSH
- Apoptosis immunology MeSH
- Bacterial Adhesion MeSH
- Bacterial Proteins genetics MeSH
- Cell Culture Techniques MeSH
- Cytoprotection genetics MeSH
- Embryo, Mammalian metabolism MeSH
- Endothelial Cells microbiology MeSH
- Financing, Organized MeSH
- Humans MeSH
- Membrane Proteins genetics deficiency MeSH
- Neisseria meningitidis pathogenicity MeSH
- Fimbriae Proteins genetics deficiency MeSH
- Flow Cytometry MeSH
- RNA, Complementary MeSH
- Oligonucleotide Array Sequence Analysis MeSH
- Signal Transduction MeSH
- Gene Expression Profiling MeSH
- Up-Regulation MeSH
- Umbilical Veins cytology MeSH
- Inflammation genetics MeSH
- Check Tag
- Humans MeSH
