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p38α MAP kinase promotes asthmatic inflammation through modulation of alternatively activated macrophages
Li-Nian Huang 1,† , Lei Sun 2,† , Li-Ming Liu 1,† , Hui-Hui Zhang2, Zhong-Bo Liang1, Yan Rui1, Jun-Feng Hu1, Yong Zhang1, John W.Christman 3,* , and Feng Qian 1,2,3,*
1 Department of Respiration and Critical Care Medicine, First Affiliated Hospital of Bengbu Medical College, Anhui Province Key Laboratory of Translational Cancer Research, Bengbu Medical College, Bengbu 233004,
China
2 Engineering Research Center of Cell & Therapeutic Antibody, Ministry of Education, School of Pharmacy, Shanghai Jiao Tong University, Shanghai 200240, China
3 Department of Internal Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine, The Ohio State University, Columbus, OH 43210-1252, USA
These authors contributed equally to this work.
*Correspondence to:Feng Qian, E-mail:fengqian@sjtu.edu.cn; John W. Christman, E-mail: john.christman@osumc.edu
J Mol Cell Biol, Volume 11, Issue 12, December 2019, 1095-1097,  https://doi.org/10.1093/jmcb/mjz054

Asthma is characterized by reversible airflow obstruction, bronchial hyper-reactivity, and chronic airway remodeling (Al-Muhsen et al., 2011). Pulmonary macrophages have been implicated in asthmatic inflammation (Lee et al., 2015; Qian et al., 2015). The p38 mitogen-activated protein kinase (MAPK) plays an essential role in inflammation, but its role in asthma has not been determined (Kim et al., 2008). Here, our data show that macrophage-specific p38α MAPK-deficient mice displayed attenuated asthmatic inflammation in response to three allergens (dust mite, ragweed, and Aspergillus; DRA). Furthermore, we found that the protective effect was strongly associated with a reduction in the alternatively activated macrophage (AAM) polarization in vivo and in vitro. Taken together, our data indicate that p38α MAPK in macrophages contributes to AAM polarization and could be a therapeutic target for asthma.