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In Vitro Characterization of the Microglial Inflammatory Response to Streptococcus suis , an Important Emerging Zoonotic Agent of Meningitis
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| Zeitschriftentitel: | Infection and Immunity |
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| Personen und Körperschaften: | , , , , , , , |
| In: | Infection and Immunity, 78, 2010, 12, S. 5074-5085 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Society for Microbiology
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| Schlagwörter: |
| Zusammenfassung: | <jats:title>ABSTRACT</jats:title> <jats:p> <jats:italic>Streptococcus suis</jats:italic> is an important swine and human pathogen responsible for septicemia and meningitis. <jats:italic>In vivo</jats:italic> research in mice suggested that in the brain, microglia might be involved in activating the inflammatory response against <jats:italic>S. suis</jats:italic> . The aim of this study was to better understand the interactions between <jats:italic>S. suis</jats:italic> and microglia. Murine microglial cells were infected with a virulent wild-type strain of <jats:italic>S. suis</jats:italic> . Two isogenic mutants deficient at either capsular polysaccharide (CPS) or hemolysin production were also included. CPS contributed to <jats:italic>S. suis</jats:italic> resistance to phagocytosis and regulated the inflammatory response by hiding proinflammatory components from the bacterial cell wall, while the absence of hemolysin, a potential cytotoxic factor, did not have a major impact on <jats:italic>S. suis</jats:italic> interactions with microglia. Wild-type <jats:italic>S. suis</jats:italic> induced enhanced expression of Toll-like receptor 2 by microglial cells, as well as phophotyrosine, protein kinase C, and different mitogen-activated protein kinase signaling events. However, cells infected with the CPS-deficient mutant showed overall stronger and more sustained phosphorylation profiles. CPS also modulated inducible nitric oxide synthase expression and further nitric oxide production from <jats:italic>S. suis</jats:italic> -infected microglia. Finally, <jats:italic>S. suis</jats:italic> -induced NF-κB translocation was faster for cells stimulated with the CPS-deficient mutant, suggesting that bacterial cell wall components are potent inducers of NF-κB. These results contribute to increase the knowledge of mechanisms underlying <jats:italic>S. suis</jats:italic> inflammation in the brain and will be useful in designing more efficient anti-inflammatory strategies for meningitis. </jats:p> |
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| Umfang: | 5074-5085 |
| ISSN: |
0019-9567
1098-5522 |
| DOI: | 10.1128/iai.00698-10 |