Journal Article

Pathogenic Neisseriae: Complexity of Pathogen-Host Cell Interplay

Thomas F. Meyer

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 28, issue 3, pages 433-441
Published in print March 1999 | ISSN: 1058-4838
Published online March 1999 | e-ISSN: 1537-6591 | DOI: https://dx.doi.org/10.1086/515160
Pathogenic Neisseriae: Complexity of Pathogen-Host Cell Interplay

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Recent studies have provided insight into the function of important neisserial adhesins (pili and Opa) and their interaction with cellular receptors, including members of heparan sulfate proteoglycan, CD66, and integrin receptor families. These interactions not only allow colonization of the human mucosa but also stimulate cellular signaling cascades involving phosphatidylcholine-dependent phospholipase C, acidic sphingomyelinase and protein kinase C in epithelial cells, and Src-related kinases, Rac1, p21-activated kinase, and Jun N-terminal kinase in phagocytic cells. Activation of these pathways is essential for cellular entry and intracellular accommodation of the pathogens but also leads to early induction of cytokine release, thus priming the immune response. Detailed knowledge of the cellular signaling cascades that are activated by infection will aid us in applying both current and novel interfering drugs (in addition to classical antibiotic therapy) as therapy and prophylaxis for persistent or otherwise difficult-to-treat bacterial infections, including periodontal infections.

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Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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