PMID- 20497712 OWN - NLM STAT- MEDLINE DCOM- 20100913 LR - 20100525 IS - 2542-5641 (Electronic) IS - 0366-6999 (Linking) VI - 123 IP - 8 DP - 2010 Apr 20 TI - Th1 immunity is not required for the effect of lipopolysaccharide exposure on modifying asthmatic responses of mice before sensitization. PG - 1047-51 AB - 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. FAU - Wu, Jing AU - Wu J AD - Department of Immunology and Ecsomatics, Anhui University of Science and Technology, Huainan, China. FAU - Hu, Dong AU - Hu D FAU - DU, Jiu-wei AU - DU JW FAU - Tao, Xin-rong AU - Tao XR FAU - Qi, Xin-lan AU - Qi XL FAU - Zhang, Rong-bo AU - Zhang RB LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - China TA - Chin Med J (Engl) JT - Chinese medical journal JID - 7513795 RN - 0 (Cytokines) RN - 0 (Lipopolysaccharides) RN - 0 (Toll-Like Receptor 4) SB - IM MH - Animals MH - Asthma/chemically induced/*immunology MH - Bronchoalveolar Lavage Fluid/immunology MH - Cytokines/*immunology/metabolism MH - Dendritic Cells/immunology MH - Dermatophagoides farinae/immunology MH - Female MH - Lipopolysaccharides/*immunology MH - Mice MH - Mice, Inbred BALB C MH - Reverse Transcriptase Polymerase Chain Reaction MH - Th1 Cells/immunology MH - Th2 Cells/*immunology MH - Toll-Like Receptor 4/genetics EDAT- 2010/05/26 06:00 MHDA- 2010/09/14 06:00 CRDT- 2010/05/26 06:00 PHST- 2010/05/26 06:00 [entrez] PHST- 2010/05/26 06:00 [pubmed] PHST- 2010/09/14 06:00 [medline] PST - ppublish SO - Chin Med J (Engl). 2010 Apr 20;123(8):1047-51.