title: Toll-like receptor expression on peripheral blood mononuclear cells in asthmatics; implications for asthma management.
abstract: BACKGROUND
  Accumulating evidence indicates that cells expressing Toll-like receptors (TLRs) play an important role in allergic diseases. The authors undertook this study to explore the hypothesis that TLR-mediated inflammatory signals are important from the perspective of asthma management.
  
  
  METHODS
  The expressions of TLR1, TLR2, TLR3, TLR4, TLR6, and TLR9 and levels of pro-inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, IL-8, and IFN-gamma) on the peripheral blood mononuclear cells (PBMCs) of 36 stable asthmatics on treatment (the on-treatment group), 15 asthmatics (the treatment-naïve group) before and after a 7-day course of oral prednisolone (30 mg/day), and on the PBMCs of 15 healthy controls were measured after in vitro stimulation using TLR-specific ligands.
  
  
  RESULTS
  In the on-treatment group, TLR1, TLR2, TLR6, and TLR9 expressions on PBMCs were significantly different between asthmatics and controls. And the expression of TLR4 on PBMCs and TNF-alpha production stimulated by lipopolysaccharide (LPS), were significantly higher in mild to moderate than in severe asthmatics. Interestingly, in the treatment-naïve group, short-term prednisolone significantly increased LPS-induced TNF-alpha and IFN-gamma productions by PBMCs.
  
  
  CONCLUSIONS
  TLR-mediated inflammatory signals contribute to the development and severity of asthma and are not reduced by glucocorticoid treatment, which suggests that a TLR-specific antagonist and glucocorticoid are required for the effective control of airway inflammation in asthmatics.
authors.affiliation: Department of Internal Medicine, Seoul National University, 28 Yongondong, Chongno-gu, Seoul, 110-744, Republic of Korea.
authors.forename: Eunyoung
authors.initials: E
authors.lastname: Chun
authors.forename: So-Hee
authors.initials: SH
authors.lastname: Lee
authors.forename: Soo-Yeon
authors.initials: SY
authors.lastname: Lee
authors.forename: Eun-Jin
authors.initials: EJ
authors.lastname: Shim
authors.forename: Sang-Heon
authors.initials: SH
authors.lastname: Cho
authors.forename: Kyung-Up
authors.initials: KU
authors.lastname: Min
authors.forename: You-Young
authors.initials: YY
authors.lastname: Kim
authors.forename: Heung-Woo
authors.initials: HW
authors.lastname: Park
mesh_terms: D000328:Adult; D000368:Aged; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D002478:Cells, Cultured; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004075:Diglycerides / Q000494:pharmacology; D018450:Disease Progression; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D055666:Lipopeptides / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009842:Oligopeptides / Q000494:pharmacology; D010457:Peptidoglycan / Q000494:pharmacology; D011239:Prednisolone / Q000008:administration & dosage* / Q000009:adverse effects; D051193:Toll-Like Receptors / Q000235:genetics / Q000276:immunology / Q000378:metabolism*
chemical_list: D016207:Cytokines; D004075:Diglycerides; C460864:FSL-1 lipoprotein, synthetic; D018836:Inflammation Mediators; D055666:Lipopeptides; D008070:Lipopolysaccharides; D009842:Oligopeptides; C508075:Pam(3)CSK(4) peptide; D010457:Peptidoglycan; D051193:Toll-Like Receptors; D011239:Prednisolone