期刊
CYTOKINE
卷 99, 期 -, 页码 114-123出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2017.08.022
关键词
IL-36; Human lung fibroblast; Human bronchial epithelial cells; Lung; Inflammation
资金
- National Natural Science Foundation of China [81370110, 81572038]
- Chongqing Science and Technology Commission Grant for Distinguished Young Scholars of Chongqing [cstc2014jcyjjq10002]
- Youth Top-notch Support Plan of Chongqing Program
- Training Program of the Research grant of Chongqing Medical University [201409]
IL-36 alpha, IL-36 beta and IL-36 gamma are cytokine members of IL-1 family. Although IL-36 expression was observed in human lung during pulmonary infections, it remains unknown whether IL-36 could act directly on lung tissue cells during pulmonary inflammatory responses. In this study, we showed that IL-36 receptor was expressed in human lung fibroblasts and bronchial epithelial cells. Correspondingly, IL-36 alpha, IL-36 beta or IL-36 gamma up-regulated gene expression of cytokine IL-6 and chemokine CXCL8 in human lung fibroblasts and bronchial epithelial cells, and promoted IL-6 and CXCL8 release from human lung fibroblasts and bronchial epithelial cells. The production of IL-6 and CXCL8 in these lung tissues cells induced by IL-36 alpha, IL-36 beta or IL-36 gamma was regulated by p38MAPK, ERK or Akt signaling pathways. Taken together, the above results suggest that IL-36-mediated IL-6 and CXCL8 production in human lung fibroblasts and bronchial epithelial cells may be involved in pulmonary inflammation especially caused by bacterial or viral infections.
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