lipoteichoic-acid and Nasal-Polyps

To investigate the anti-inflammatory effect of levocetrizine (LCEZ) on the intracellular adhesion molecule-1 (ICAM-1) in human nasal epithelial cells stimulated by TLR3 and further analyze the anti-inflammatory mechanism of LCEZ in the MyD88-independent pathway before NF-κB is activated.. A primary culture of human nasal epithelial cells (HNECs) was generated from nasal polyps. After stimulation of epithelial cells with LTA, double-stranded RNA (dsRNA), and LPS, reverse transcription-polymerase chain reaction (RT-PCR) was performed at 1, 6, and 24 h to clarify the optimal stimulation of ICAM-1 in HNECs. To investigate the anti-inflammatory effects of LCEZ, HNECs were pretreated with three different concentrations of LCEZ (500, 50, and 5 nM) for 2 h. HNECs were washed and then stimulated with dsRNA. At 1, 6, and 24 h after stimulation, the level of ICAM-1 was measured by RT-PCR and ELISA. Western blots for TRIF and RIP were performed.. The level of ICAM-1 was significantly elevated by dsRNA. Pretreatment with LCEZ decreased the secretion of ICAM-1, which was observed in RT-PCR and Western blots but not in ELISA analyses. The expression of TRIF and RIP, measured by Western blot, was decreased by pretreatment with LCEZ.. The activation of HNECs by TLRs (especially TLR3) could trigger an inflammatory process, which might be inhibited by LCEZ through the suppression of TRIF and RIP proteins.

Topics: Adaptor Proteins, Vesicular Transport; Anti-Inflammatory Agents; Blotting, Western; Cells, Cultured; Cetirizine; Enzyme-Linked Immunosorbent Assay; Humans; Intercellular Adhesion Molecule-1; Lipopolysaccharides; Nasal Mucosa; Nasal Polyps; Receptor-Interacting Protein Serine-Threonine Kinases; Reverse Transcriptase Polymerase Chain Reaction; RNA, Double-Stranded; Teichoic Acids; Toll-Like Receptor 3

Increasing evidence points toward a modifying role of Staphylococcus aureus and its products in the pathogenesis of nasal polyposis.. The aim of this study was to investigate cytokine and mediator production after stimulation with S aureus-derived proteins enterotoxin B, protein A, and lipoteichoic acid in nasal polyp and control inferior turbinate tissue.. Tissue fragments were stimulated with RPMI (negative control), enterotoxin B, protein A, and lipoteichoic acid for 30 minutes and 24 hours. Supernatants were measured by multiplex for proinflammatory cytokines (IL-1beta, TNF-alpha) and T-cell and subset-related cytokines (IFN-gamma, IL-2, IL-4, IL-5, IL-8, IL-10, IL-12p70, IL-13). Histamine, TGF-beta1, cysteinyl leukotrienes, and prostaglandin D(2) were analyzed by ELISA.. Thirty minutes of protein A stimulation resulted in a significant increase of histamine, leukotrienes, and prostaglandin D(2). Enterotoxin B stimulation over a period of 24 hours induced a significant increase of IL-1beta, TNF-alpha, IFN-gamma, IL-2, IL-4, IL-5, IL-10, and IL-13 in both groups, with this increase significantly higher in nasal polyps compared with controls.. We here show that S aureus products have various effects on mucosal tissues: surface protein A induces mast cell degranulation, whereas enterotoxins induce the release of cytokines, with a T(H)2-skewed pattern in nasal polyps, supporting the stimulatory role of superantigens in the development of this inflammatory disease.

Topics: Adult; Aged; Cytokines; Enterotoxins; Female; Humans; Lipopolysaccharides; Lymphocyte Activation; Male; Mast Cells; Middle Aged; Nasal Mucosa; Nasal Polyps; Staphylococcal Protein A; Staphylococcus aureus; T-Lymphocytes; Teichoic Acids; Turbinates