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Mediators of Inflammation
Volume 2006 (2006), Article ID 84829, 8 pages
Research Communication

LIF Upregulates Expression of NK-1R in NHBE Cells

1Department of Respiratory Medicine, Xiangya Hospital of Central South University, Hunan Province, Changsha 410008, China
2Department of Respiratory Medicine, Changsha Central Hospital, Hunan Province, Changsha 410008, China
3Third Institute of Oceanography, SOA, Fujian Province, Xiamen 361005, China

Received 24 March 2006; Revised 30 July 2006; Accepted 7 August 2006

Copyright © 2006 Cheng-Ping Hu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Leukemia inhibitory factor (LIF), a cytokine at the interface between neurobiology and immunology, is mainly mediated through JAK/STAT pathway and MAPK/ERK pathway. Evidence suggested LIF is related to the higher expression of neurokinin-1 receptor (NK-1R) in asthma. In this study, the immunohistochemistry stain showed the expressions of NK-1R, LIF, p-STAT3, and p-ERK1/2 in the lung tissues of allergic rats were increased compared with the controls, and the main positive cell type was airway epithelial cell. Normal human bronchial epithelial cells were treated with LIF in the presence or absence of AG490 (JAK2 inhibitor), PD98059 (MEK inhibitor), and the siRNA against STAT3. Western blot and RT-PCR indicated that LIF induced the expression of NK-1R, which was inhibited by the inhibitors mentioned above. No significant interaction was found between JAK/STAT pathway and MAPK/ERK pathway. In summary, bronchial epithelial cell changes in asthma are induced by LIF which promotes the expression of NK-1R, and JAK/STAT pathway and MAPK/ERK pathway may participate in this process.