草綠色鏈球菌葡萄糖傳遞酶與內皮細胞的交互作用參與感染性心內膜炎的免疫致病機制

葉秋月

doi:10.6342/NTU.2006.01403

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草綠色鏈球菌葡萄糖傳遞酶與內皮細胞的交互作用參與感染性心內膜炎的免疫致病機制

Viridans streptococcal glucosyltransferases–endothelial cell interactions in the immunopathogenesis of infective endocarditis

葉秋月 , Ph.D　　Advisor：賈景山　　

繁體中文 DOI： 10.6342/NTU.2006.01403

轉糖鏈球菌；感染性心內膜炎；葡萄糖傳遞酶細胞激素；內皮細胞；心臟纖維母細胞；艱難梭狀桿菌； Streptococcus mutans ； infective endocarditis ； glucosyltransferase ； interleukin ； endothelial cell ； cardiac fibroblast ； Clostridium difficile

Abstract │ Reference (301) │ Times Cited (2) │ Altmetrics

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Infective endocarditis (IE), a microbial infection in the heart valves, is characterized by vegetation formation and chronic endocardial inflammation. In the present study, we examined the role of glucosyltransferases (GTFs) found in viridans streptococci-induced infective endocarditis. GTFs were discovered in several IE-inducing streptococcal species, and presented as either the bacterial surface or extracellular enzyme, to synthesize glucan that cause bacterial aggregation and biofilm formation on tooth surfaces. GTFs were also identified to be modulins of IL-6 production in monocytes of human or rat. When treated on HUVEC, both bacteria-bound and -free GTFs could induce IL-6 and adhesion molecule expression through NF-kB activation. Activated endothelial cells enhance adhesion of monocytes and such adhesion can also be achieved by treating the cells with a mixture containing IL-6 and IL-6Rα. Furthermore, we demonstrate that GTF is detected in situ and induces IL-6 synthesis during acute phase of S. mutans-induced rat experimental endocarditis. In clinical specimens from viridans streptococci induced endocarditis, secretion of pro-inflammatory cytokines was detected on valvular, neocapillary endothelial cells, infiltrated macrophages and cardiac fibroblasts. Cardiac fibroblasts cultured in vitro can be activated synergistically by IL-1β and TNF-α, released from GTF-activated monocytes, to release MCP-1. Taken together, we propose a mechanism for endocardial inflammation during IE for recruitment and retention of monocytes, the former may be activated by bacterial modulins on endothelial lining, while, the latter, may be maintained by cardiac fibroblasts through cytokines and chemokines. The C-terminal repetitive domain of Clostridium difficile toxin A (ARU) is homologous to GTF and exhibites adjuvant activity in mucosal immunity. In second part of this study, we demonstrate that ARU is sufficient to induce IL-6, IL-8 and MCP-1 production in endothelial cells through serum- and calcium-dependent manner. Inhibition results demonstrate that cytokine production in ARU-activated HUVEC is through PI3K、PKC、PTK、MAPKs and NF-kB activation. Both IL-8 and MCP-1 trigger leukocytes chemotaxis in vitro. These results suggest that mucosal adjuvant activity of C-terminus of TcdA may also attribute to the interaction of endothelial cells to release IL-6, which is important for maturating plasma cells. Take together; we hypothesized that the C-terminal repeates of GTFs, similar to ARU, might be involved in the binding of endothelial cells.

Reference ( 301 ) 〈TOP〉

1. Abo, H., T. Matsumura, T. Kodama, H. Ohta, K. Fukui, K. Kato, and H. Kagawa. 1991. Peptide sequences for sucrose splitting and glucan binding within Streptococcus sobrinus glucosyltransferase (water-insoluble glucan synthetase). J. Bacteriol. 173:989-996.
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2. Agocha, A. E. and M. Eghbali-Webb. 1997. A simple method for preparation of cultured cardiac fibroblasts from adult human ventricular tissue. Mol. Cell Biochem. 172:195-198.
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4. Akira, S. and H. Hemmi. 2003. Recognition of pathogen-associated molecular patterns by TLR family. Immunol. Lett. 85:85-95.
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5. Al Okla, S., C. Chatenay-Rivauday, J. P. Klein, and D. Wachsmann. 1999. Involvement of alpha5beta1 integrins in interleukin 8 production induced by oral viridans streptococcal protein I/IIf in cultured endothelial cells. Cell Microbiol. 1:157-168.
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7. Alexopoulou, L., A. C. Holt, R. Medzhitov, and R. A. Flavell. 2001. Recognition of double-stranded RNA and activation of NF-kappaB by Toll-like receptor 3. Nature. 413:732-738.
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