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Lipooligosaccharide structure contributes to multiple steps in the virulence of Neisseria meningitidis.: LOS structure and meningococcal virulence
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
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2006 In: Infection and Immunity, Vol. 74, no 2, 1360-1367 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2006. Vol. 74, no 2, 1360-1367 p.
URN: urn:nbn:se:uu:diva-95663OAI: oai:DiVA.org:uu-95663DiVA: diva2:169969
Available from: 2007-04-03 Created: 2007-04-03Bibliographically approved
In thesis
1. Receptor Interactions Between Pathogenic Bacteria and Host Cells
Open this publication in new window or tab >>Receptor Interactions Between Pathogenic Bacteria and Host Cells
2007 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

This thesis focuses on host and pathogen specific interactions during invasive disease. We have investigated the role and impact of different virulence factors of Neisseria gonorrhoeae, N. meningitidis and Streptococcus pyogenes on host epithelial cells and in vivo.

N. gonorrhoeae cause the sexually transmitted disease gonorrhoea and N. meningitidis is the most common cause of bacterial meningitis and may be leathal to the host within hours of infection. The neisserial type IV pili were shown to have an important impact on host cells for the induction of pro-inflammatory and other cellular defence transcriptional responses. Furthermore, N. meningitidis generally induced an earlier response compared to N. gonorrhoeae, probably as a result of the meningococcal capsule. The role of N. meningitidis serogroup B lipooliogsaccharide was investigated during invasive disease. Bacterial invasion of host cells and blood survival as well as virulence in vivo was dependent on the integrity of the LOS structure.

S. pyogenes may cause a variety of diseases ranging from uncomplicated diseases such as 'strep-throat' to more severe invasive diseases such as necrotizing fasciitis and streptococcal toxic shock syndrome. S. pyogenes ScpC protease degrade interleukin 8 during necrotizing fasciitis. We investigated the role of ScpC in systemic disease and observed enhanced virulence by bacteria unable to degrade IL-8. Following an intravenous infection of mice pro-inflammatory cytokines and complement activation was induced by the ScpC negative mutant compared to the wild-type and correlated with higher bacteremia. These data indicate that the precense of the ScpC protease has an important impact on the host for the outcome of streptococcal sepsis. Another phagocytic escape mechanism of S. pyogenes is their ability to coat themselves with host proteins. We observed that released complement control protein, CD46, bound to the streptococcal cell surface. CD46 has been shown to interact with the streptococcal M protein and have now been found to bind to the surface of the bacteria in a growth phase dependent manner. We observed a more aggressive disease development in CD46 transgenic mice after an intravenous infection with an M6 serotype, resulting in higher mortality of CD46 transgenic mice compared with control mice. These data indicate that CD46 may confer a protection to the streptococci during early stage of systemic infection and contributes to the understanding of immune evsion of S. pyogenes.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2007. 78 p.
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 247
Microbiology, Type IV pili, Lipooligosaccharide, ScpC protease, CD46, Mikrobiologi
urn:nbn:se:uu:diva-7782 (URN)978-91-554-6847-7 (ISBN)
Public defence
2007-04-26, B7: 101a, Biomedicinskt Centrum, Husargatan 3, Uppsala, 10:00
Available from: 2007-04-03 Created: 2007-04-03Bibliographically approved

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