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Oral\n            <jats:italic>V. parvula<\/jats:italic>\n            is involved in the development of early periodontal disease as well as different types of serious infections. Present data on molecular mechanisms responsible for innate immune response against\n            <jats:italic>Veillonella<\/jats:italic>\n            are very scanty. The aim of this study was to investigate the Toll-like receptor (TLR) pathways responsible for\n            <jats:italic>V. parvula<\/jats:italic>\n            lipopolysaccharide (LPS) and to identify the intracellular pathways induced by this recognition.\n            <jats:italic>V. parvula<\/jats:italic>\n            LPS stimulated tumor necrosis factor alpha (TNF-\u03b1) and interleukin-6 (IL-6) release in human peripheral blood mononuclear cells (PBMC) in a dose-dependent manner. Pretreatment of cells with a TLR4 antagonist significantly reduced TNF-\u03b1 and IL-6 production in PBMC stimulated with either\n            <jats:italic>Veillonella<\/jats:italic>\n            or\n            <jats:italic>Escherichia coli<\/jats:italic>\n            LPS. However,\n            <jats:italic>V. parvula<\/jats:italic>\n            LPS was 10- to 100-fold less active than\n            <jats:italic>E. coli<\/jats:italic>\n            LPS for cytokine induction. TNF-\u03b1, IL-1\u03b2, IL-6, and IL-10 were released in wild-type and TLR2\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            , but not TLR4\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            , mouse macrophage cultures.\n            <jats:italic>V. parvula<\/jats:italic>\n            LPS was able to activate the human PBMC p38 mitogen-activated protein kinase (MAPK). A specific p38 MAPK inhibitor strongly inhibited\n            <jats:italic>V. parvula<\/jats:italic>\n            LPS-induced TNF-\u03b1, IL-1\u03b2, IL-6, and IL-10. In conclusion,\n            <jats:italic>V. parvula<\/jats:italic>\n            LPS is able to induce cytokine production in both human and murine in vitro models, although it is less effective than\n            <jats:italic>Enterobacteriaceae<\/jats:italic>\n            LPS.\n            <jats:italic>V. parvula<\/jats:italic>\n            LPS-stimulated cytokine induction, as well as p38 MAPK activation, are TLR4-dependent features.\n          <\/jats:p>","DOI":"10.1128\/cvi.00310-09","type":"journal-article","created":{"date-parts":[[2009,10,15]],"date-time":"2009-10-15T01:42:10Z","timestamp":1255570930000},"page":"1804-1809","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":69,"title":["Receptor Recognition of and Immune Intracellular Pathways for\n            <i>Veillonella parvula<\/i>\n            Lipopolysaccharide"],"prefix":"10.1128","volume":"16","author":[{"given":"Giovanni","family":"Matera","sequence":"first","affiliation":[{"name":"Institute of Microbiology, Department of Medical Sciences, University of Cantanzaro, Catanzaro, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valentina","family":"Muto","sequence":"additional","affiliation":[{"name":"Institute of Microbiology, Department of Medical Sciences, University of Cantanzaro, Catanzaro, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Vinci","sequence":"additional","affiliation":[{"name":"Institute of Microbiology, Department of Medical Sciences, University of Cantanzaro, Catanzaro, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emilia","family":"Zicca","sequence":"additional","affiliation":[{"name":"Institute of Microbiology, Department of Medical Sciences, University of Cantanzaro, Catanzaro, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shahla","family":"Abdollahi-Roodsaz","sequence":"additional","affiliation":[{"name":"Rheumatology Research &amp; Advanced Therapeutics, Department of Rheumatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank L.","family":"van de Veerdonk","sequence":"additional","affiliation":[{"name":"Department of Medicine"},{"name":"Nijmegen Institute for Infection, Inflammation and Immunity"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bart-Jan","family":"Kullberg","sequence":"additional","affiliation":[{"name":"Department of Medicine"},{"name":"Nijmegen Institute for Infection, Inflammation and Immunity"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Carla","family":"Liberto","sequence":"additional","affiliation":[{"name":"Institute of Microbiology, Department of Medical Sciences, University of Cantanzaro, Catanzaro, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jos W. 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