title: Th1 immunity is not required for the effect of lipopolysaccharide exposure on modifying asthmatic responses of mice before sensitization.
abstract: BACKGROUND
  Disequilibrium of Th1/Th2 is known as an important cause of allergic asthma with a biased Th2 type response. It has been shown that lipopolysaccharide (LPS) administration during post-sensitization modified the inflammation of asthma via upregulating the Th1 response that decrease the Th2 immunity. We would like to know if, during pre-sensitization, the elevated Th1 response is necessary for LPS exposure to modify the asthmatic response.
  
  
  METHODS
  During pre- or post-sensitization, 40 microg LPS were intraperitoneal injected (i.p.) to asthmatic mice sensitized and challenged by Dermatophagoides farinae (D. farinea). Inflammation was assessed by examining bronchoalveolar lavage fluid (BALF) for the number and identity of cells and by cytokine titers measured by ELISA. Semi-quantified RT-PCR was used to evaluate the level of Toll-like receptor 4 (TLR4) mRNA in dendritic cells (DCs) from bone marrow (BMDCs).
  
  
  RESULTS
  These investigations demonstrated that LPS exposure during pre-sensitization inhibited the Th2 cytokine and inflammatory infiltration, the same as with LPS exposure during post-sensitization in allergic asthma mice. Contrary to post-sensitization LPS exposure, the Th1 cytokines were not upregulated by pre-sensitization with LPS. Finally, the study failed to show any significant difference between TLR4 mRNA expressed in BMDCs with the two times of LPS exposure.
  
  
  CONCLUSIONS
  Our data suggest that elevated Th1 immunity is not required for the modification of the Th2 response induced by LPS exposure during pre-sensitization in asthmatic mice and that pre-sensitization differs from post-sensitization. Immune modulation with treatment is independent of TLR4 expression in BMDCs. This study implicates a potential way to protect from allergic disease and an inflammatory response.
authors.affiliation: Department of Immunology and Ecsomatics, Anhui University of Science and Technology, Huainan, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Wu
authors.forename: Dong
authors.initials: D
authors.lastname: Hu
authors.forename: Jiu-wei
authors.initials: JW
authors.lastname: DU
authors.forename: Xin-rong
authors.initials: XR
authors.lastname: Tao
authors.forename: Xin-lan
authors.initials: XL
authors.lastname: Qi
authors.forename: Rong-bo
authors.initials: RB
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D016207:Cytokines / Q000276:immunology* / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology; D040001:Dermatophagoides farinae / Q000276:immunology; D005260:Female; D008070:Lipopolysaccharides / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology*; D051197:Toll-Like Receptor 4 / Q000235:genetics
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D051197:Toll-Like Receptor 4