title: Lipoteichoic acid from Staphylococcus aureus enhances allergen-specific immunoglobulin E production in mice.
abstract: BACKGROUND
  Our previous study demonstrated that lipoteichoic acid (LTA) from Staphylococcus aureus induced T helper type 2 (Th2)-prone dermatitis resembling that seen in atopic dermatitis (AD) patients in mice sensitized percutaneously with an allergen. However, the effects of LTA on allergen-specific IgE production in such sensitized mice have not been elucidated.
  
  
  OBJECTIVE
  The purpose of this study was to determine the effects of LTA from S. aureus on allergen-specific IgE production in mice sensitized percutaneously with a house dust mite antigen (MA).
  
  
  METHODS
  Mice were sensitized with a single topical application of MA and/or LTA to barrier-disrupted abdominal skin. One to 5 weeks later, MA-specific IgE antibodies in sera from sensitized mice were detected by an enzyme-linked immunosorbent assay (ELISA). Expression of B7.1 (CD80), B7.2 (CD86) and CD40L molecules by CD40-positive (CD40+) and CD4-positive (CD4+) cells in the lymph nodes of sensitized mice were analysed by flow-cytometry (FACS).
  
  
  RESULTS
  Simultaneous sensitization with MA and LTA increased IgE production 3 weeks later, significantly more than sensitization with MA alone. FACS analysis of CD40+ cells in the lymph nodes from sensitized mice showed that simultaneous sensitization with MA and LTA did not enhance CD80- or CD86-expression by antigen-presenting cells such as B lymphocytes and dendritic cells more than sensitization with MA alone. However, analysis of CD4+ cells in the lymph nodes showed that simultaneous sensitization with MA and LTA increased the number of CD40L-expressing Th cells more than sensitization with MA alone.
  
  
  CONCLUSIONS
  These results suggest that LTA enhances allergen-specific IgE production by a mechanism associated with up-regulation of CD40L-expressing Th cells and this might explain the role of skin colonization with S. aureus in AD patients.
authors.affiliation: Department of Immunobiology, Meiji Pharmaceutical University, Tokyo, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Matsui
authors.forename: A
authors.initials: A
authors.lastname: Nishikawa
mesh_terms: D000485:Allergens / Q000276:immunology*; D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D039741:Antigens, Dermatophagoides; D060829:Arthropod Proteins; D018122:B7-1 Antigen / Q000032:analysis; D051940:B7-2 Antigen; D023201:CD40 Ligand / Q000032:analysis; D003546:Cysteine Endopeptidases; D005260:Female; D005434:Flow Cytometry; D006969:Hypersensitivity, Immediate / Q000276:immunology*; D007073:Immunoglobulin E / Q000096:biosynthesis*; D018793:Interleukin-13 / Q000235:genetics; D015847:Interleukin-4 / Q000235:genetics; D008070:Lipopolysaccharides / Q000276:immunology*; D008562:Membrane Glycoproteins / Q000032:analysis; D051379:Mice; D008807:Mice, Inbred BALB C; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013047:Specific Pathogen-Free Organisms; D013682:Teichoic Acids / Q000276:immunology*
chemical_list: D000485:Allergens; D015703:Antigens, CD; D039741:Antigens, Dermatophagoides; D060829:Arthropod Proteins; D018122:B7-1 Antigen; D051940:B7-2 Antigen; C497965:Cd86 protein, mouse; D018793:Interleukin-13; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D013682:Teichoic Acids; D023201:CD40 Ligand; D015847:Interleukin-4; D007073:Immunoglobulin E; C009900:lipoteichoic acid; D003546:Cysteine Endopeptidases; C451159:Dermatophagoides farinae antigen f 1