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The transcription factor PU.1 promotes alternative macrophage polarization and asthmatic airway inflammation

Journal of Molecular Cell Biology 2015年第6期7卷 557-567页

作者： Feng Qian Jing Deng Yong Gyu Lee Jimmy Zhu Manjula Karpurapu Sangwoon Chung Jun-Nian Zheng Lei Xiao Gye Young Park John W.Christman School of Pharmacy Engineering Research Center of Cell&Therapeutic AntibodyMinistry of EducationShanghai Jiao Tong UniversityShanghaiChina Department of Internal Medicine Section of PulmonaryAllergyCritical Careand Sleep MedicineThe Ohio State UniversityColumbusUSA Department of Physiology and Biophysics College of MedicineUniversity of Illinois at ChicagoChicagoUSA Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy Cancer InstituteXuzhou Medical CollegeXuzhouChina Department of Medicine Section of PulmonaryCritical Careand Sleep MedicineUniversity of Illinois at ChicagoChicagoUSA

The transcription factor PU.1 is involved in regulation of macrophage differentiation and ***,the role of PU.1 in alternatively activated macrophage(AAM)and asthmatic inflammation has yet been *** we report that PU.1 serves as a critical regulator of AAM polarization and promotes the pathological progress of asthmatic airway *** response to the challenge of DRA(dust mite,ragweed,and Aspergillus)allergens,conditional PU.1-deficient(PU/ER(T)^(+/-))mice displayed attenuated allergic airway inflammation,including decreased alveolar eosinophil infiltration and reduced production of IgE,which were associated with decreased mucous glands and goblet cell *** reduced asthmatic inflammation in PU/ER(T)^(+/-) mice was restored by adoptive transfer of IL-4-induced wild-type(WT)***,after treating PU/ER(T)^(+/-) mice with tamoxifen to rescue PU.1 function,the allergic asthmatic inflammation was significantly *** vitro studies demonstrate that treatment of PU.1-deficient macrophages with IL-4 attenuated the expression of chitinase 3-like 3(Ym-1)and resistin-like molecule alpha 1(Fizz-1),two specific markers of AAM *** addition,PU.1 expression in macrophages was inducible in response to IL-4 challenge,whichwas associated with phosphorylation of signal transducer and activator of transcription 6(STAT6).Furthermore,DRAchallenge in sensitized mice almost abrogated gene expression of Ym-1 and Fizz-1 in lung tissues of PU/ER(T)^(+/-) mice compared with WT *** data,all together,indicate that PU.1 plays a critical role in AAM polarization and asthmatic inflammation.

关键词： PU.1 alternatively activated macrophage asthmatic inflammation Th2 IL-4

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