Increased transcription of cytokine genes in human lung epithelial cells through activation of a TRPM8 variant by cold temperatures.
Increased transcription of cytokine genes in human lung epithelial cells through activation of a TRPM8 variant by cold temperatures.
复制标题
通过低温激活 TRPM8 变体，增加人肺上皮细胞中细胞因子基因的转录。
DOI：
10.1152/ajplung.00072.2008
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Yost,GaroldS
中科院分区：
文献类型：
--
作者：
Sabnis,AshwiniS;Reilly,ChristopherA;Veranth,JohnM;Yost,GaroldS
Recognition of temperature is a critical element of sensory perception and allows mammals to evaluate both their external environment and internal status. The respiratory epithelium is constantly exposed to the external environment, and prolonged inhalation of cold air is detrimental to human airways. However, the mechanisms responsible for adverse effects elicited by cold air on the human airways are poorly understood. Transient receptor potential melastatin family member 8 (TRPM8) is a well-established cold- and menthol-sensing cation channel. We recently discovered a functional cold- and menthol-sensing variant of the TRPM8 ion channel in human lung epithelial cells. The present study explores the hypothesis that this TRPM8 variant mediates airway cell inflammatory responses elicited by cold air/temperatures. Here, we show that activation of the TRPM8 variant in human lung epithelial cells leads to increased expression of several cytokine and chemokine genes, including IL-1α, -1β, -4, -6, -8, and -13, granulocyte-macrophage colony-stimulating factor (GM-CSF), and TNF-α. Our results provide new insights into mechanisms that potentially control airway inflammation due to inhalation of cold air and suggest a possible role for the TRPM8 variant in the pathophysiology of asthma.
