Thl immunity is not required for the effect of lipopolysaccharide exposure on modifying asthmatic responses of mice before sensitization  

作　　者：WU Jing HU Dong DU Jiu-wei TAO Xin-rong QI Xin-lan ZHANG Rong-bo 

机构地区：[1]Department of Immunology and Ecsomatics, Medical School, Anhui University of Science and Technology, Huainan, Anhui 232001, China [2]Institute of Infectious Disease, Guangzhou No. 8 People's Hospital, Guangzhou, Guangdong 510080, China

出　　处：《Chinese Medical Journal》2010年第8期1047-1051,共5页中华医学杂志（英文版）

摘　　要：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 Thl response that decrease the Th2 immunity. We would like to know if, during pre-sensitization, the elevated Thl response is necessary for LPS exposure to modify the asthmatic response. Methods During pre- or post-sensitization, 40 IJg 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 Thl 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 Thl 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 wav to protect from allergic disease and an inflammatory response.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 Thl response that decrease the Th2 immunity. We would like to know if, during pre-sensitization, the elevated Thl response is necessary for LPS exposure to modify the asthmatic response. Methods During pre- or post-sensitization, 40 IJg 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 Thl 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 Thl 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 wav to protect from allergic disease and an inflammatory response.

关 键 词：asthma ALLERGY Th1/Th2 LIPOPOLYSACCHARIDE Toll-like receptor 4 inflammation 

分 类 号：S942.5[农业科学—水产养殖] TQ028.8[农业科学—水产科学]