title: Streptococcus gordonii promotes rapid differentiation of monocytes into dendritic cells through interaction with the sialic acid-binding adhesin.
abstract: Infective endocarditis is frequently attributed to oral streptococci. Although the pathogenetic mechanisms are not well understood, interaction between streptococci and phagocytes is thought to be important for infective endocarditis. In this study, HL-60 cell-derived monocytes were characterized following interaction with Streptococcus gordonii DL1. Exposure of monocytes to S. gordonii DL1 induced up-regulation of the dendritic cell (DC) markers CD83, CD1a, CD86, and interleukin-12, while monocyte markers PU.1 and MafB, which are typically present at low levels in mature DCs, were down-regulated. Interaction of HL-60-derived monocytes with S. gordonii DL1 was instructive for DC differentiation in the absence of released cytokines. Furthermore, neither the filtered culture medium of S. gordonii nor the hsa mutant, deficient in sialic acid-binding activity, was able to induce the differentiation of HL-60 cells. Taken together, these data suggest that monocytes stimulated with S. gordonii DL1 rapidly undergo monocyte-to-DC differentiation through interaction with the bacterial surface receptor Hsa and that this response may be the initial step in infective endocarditis by oral streptococci.
authors: Department of Microbiology, Nippon Dental University School of Life Dentistry at Tokyo, Tokyo, Japan. yumiurano@tky.ndu.ac.jp
authors: Yumiko
authors: Y
authors: Urano-Tashiro
authors: Ayako
authors: A
authors: Yajima
authors: Yukihiro
authors: Y
authors: Takahashi
authors: Kiyoshi
authors: K
authors: Konishi
mesh_terms: D018829:Adhesins, Bacterial / Q000502:physiology*; D015703:Antigens, CD / Q000032:analysis; D018949:Antigens, CD1 / Q000032:analysis; D051940:B7-2 Antigen / Q000032:analysis; D001422:Bacterial Adhesion / Q000502:physiology; D002352:Carrier Proteins / Q000502:physiology*; D002454:Cell Differentiation / Q000502:physiology; D045744:Cell Line, Tumor; D003713:Dendritic Cells / Q000502:physiology*; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000032:analysis; D006389:Hemagglutinins, Viral; D006801:Humans; D007136:Immunoglobulins / Q000032:analysis; D018664:Interleukin-12 / Q000032:analysis; D053762:Interleukin-12 Subunit p40; D015847:Interleukin-4 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D016350:Leucine Zippers; D016173:Macrophage Colony-Stimulating Factor / Q000032:analysis; D051258:MafB Transcription Factor / Q000032:analysis; D008562:Membrane Glycoproteins / Q000032:analysis; D009000:Monocytes / Q000382:microbiology*; D011518:Proto-Oncogene Proteins / Q000032:analysis; D054773:Streptococcus gordonii / Q000502:physiology*; D015534:Trans-Activators / Q000032:analysis; D000097802:CD83 Antigen; D000099232:Proto-Oncogene Protein Spi-1
chemical_list: D018829:Adhesins, Bacterial; D015703:Antigens, CD; D018949:Antigens, CD1; D051940:B7-2 Antigen; D002352:Carrier Proteins; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D006389:Hemagglutinins, Viral; D007136:Immunoglobulins; D018664:Interleukin-12; D053762:Interleukin-12 Subunit p40; D015847:Interleukin-4; D015850:Interleukin-6; D016173:Macrophage Colony-Stimulating Factor; D051258:MafB Transcription Factor; D008562:Membrane Glycoproteins; D011518:Proto-Oncogene Proteins; D015534:Trans-Activators; D000097802:CD83 Antigen; D000099232:Proto-Oncogene Protein Spi-1; C419393:CD1a antigen; C490407:MAFB protein, human; C450840:hsa protein, Streptococcus gordonii