MaxiK Blockade Selectively Inhibits the Lipopolysaccharide-Induced IκB-α/NF-κB Signaling Pathway in Macrophages

摘要: Macrophages have a pivotal function in innate immunity against bacterial infections. They are present all body compartments and able to detect invading microorganisms with high sensitivity. LPS (endotoxin) of Gram-negative bacteria is among the most potent stimuli for macrophages initiates wide panel cellular activation responses. The release mediators such as TNF-α ILs essential initiation proinflammatory antibacterial response. Here, we show that blockade large-conductance Ca2+-activated potassium channel MaxiK (BK) inhibited cytokine production from LPS-stimulated at transcriptional level. This inhibitory effect was specific stimulation affected neither nor LPS-induced cells do not express MaxiK. Investigation upstream intracellular signaling pathways induced by revealed selectively leading transcription factor NF-κB MAPK p38, whereas ERK unaffected. We data supporting proximal regulation IκB-α critically involved observed inhibition translocation. Using alveolar rats, could necessity subsequent restricted vitro-generated monocyte-derived but also can be primary cells. Thus, appears central molecule NF-κB-dependent inflammatory response LPS.