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      Treponema denticola interactions with host proteins

      research-article
      *
      Journal of Oral Microbiology
      Co-Action Publishing
      spirochetes, virulence factors, periodontal disease

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          Abstract

          Oral Treponema species, most notably T. denticola, are implicated in the destructive effects of human periodontal disease. Progress in the molecular analysis of interactions between T. denticola and host proteins is reviewed here, with particular emphasis on the characterization of surface-expressed and secreted proteins of T. denticola involved in interactions with host cells, extracellular matrix components, and components of the innate immune system.

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          Most cited references139

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          Hyaluronan as an immune regulator in human diseases.

          Accumulation and turnover of extracellular matrix components are the hallmarks of tissue injury. Fragmented hyaluronan stimulates the expression of inflammatory genes by a variety of immune cells at the injury site. Hyaluronan binds to a number of cell surface proteins on various cell types. Hyaluronan fragments signal through both Toll-like receptor (TLR) 4 and TLR2 as well as CD44 to stimulate inflammatory genes in inflammatory cells. Hyaluronan is also present on the cell surface of epithelial cells and provides protection against tissue damage from the environment by interacting with TLR2 and TLR4. Hyaluronan and hyaluronan-binding proteins regulate inflammation, tissue injury, and repair through regulating inflammatory cell recruitment, release of inflammatory cytokines, and cell migration. This review focuses on the role of hyaluronan as an immune regulator in human diseases.
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            Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2.

            Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor-2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor-kappaB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.
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              Fibronectin fibrillogenesis, a cell-mediated matrix assembly process.

              The extracellular matrix provides a framework for cell adhesion, supports cell movement, and serves to compartmentalize tissues into functional units. Fibronectin is a core component of many extracellular matrices where it regulates a variety of cell activities through direct interactions with cell surface integrin receptors. Fibronectin is synthesized by many adherent cells which then assemble it into a fibrillar network. The assembly process is integrin-dependent and fibronectin-integrin interactions initiate a step-wise process involving conformational activation of fibronectin outside and organization of the actin cytoskeleton inside. During assembly, fibronectin undergoes conformational changes that expose fibronectin-binding sites and promote intermolecular interactions needed for fibril formation. In this review, the main steps of fibronectin assembly are described and recent studies on fibronectin conformational changes are discussed.
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                Author and article information

                Journal
                J Oral Microbiol
                JOM
                Journal of Oral Microbiology
                Co-Action Publishing
                2000-2297
                21 February 2012
                2012
                : 4
                : 10.3402/jom.v4i0.9929
                Affiliations
                Department of Biologic and Materials Sciences, School of Dentistry, University of Michigan, Ann Arbor, MI, USA
                Author notes
                [* ] J. Christopher Fenno, Department of Biologic and Materials Sciences School of Dentistry, University of MichiganAnn, Arbor MI, USA. Tel: +(734) 763 3331. Fax: +(734) 647 2110. Email: fenno@ 123456umich.edu
                Article
                JOM-4-9929
                10.3402/jom.v4i0.9929
                3285142
                22368767
                8da8803b-8e90-41e0-a648-17a71265777c
                © 2012 J. Christopher Fenno.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Host-Pathogen Interactions in Bacteria

                Microbiology & Virology
                spirochetes,virulence factors,periodontal disease
                Microbiology & Virology
                spirochetes, virulence factors, periodontal disease

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