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Aim:Our previous data have shown that type Ⅱ alveolar epithelial(AEⅡ)cellsexpress neuropeptide calcitonin gene-related peptide(CGRP),and that pro-in-flammatory factor interleukin 1-β(IL-1β)induces CGRP secretion in the A549 hu-man AEⅡ cell line.In the present study,we investigated the effect of endogenousand exogenous CGRP on IL-1β-induced chemokine interleukin-8(IL-8)secretion.Methods:We used enzyme-linked immunosorbent assay(ELISA)and RT-PCR todetect IL-8 protein and mRNA levels,respectively,siRNA and the stably trans-fected cell line were used to knock down and overexpress the CGRP gene,respectively,and chemiluminescence assay was used to detect reactive oxygenspecies(ROS)formation.Results:CGRP-1 receptor antagonist hCGRP_(8-37)(0.1-1nmol·L~(-1))greatly amplified IL-1β-induced IL-8 production.The inhibition of CGRPexpression by siRNA significantly increased IL-8 secretion upon IL-1β stimulation.However,cell clones stably transfected with CGRP showed significantly inhibitedmRNA and protein levels of IL-8 induced by 1L-1β.Conclusion:These data implythat AEⅡ cell-derived CGRP suppress IL-1β-induced IL-8 secretion in an autocrine/paracrine mode.Further investigation showed that CGRP attenuated IL-1β-arousedROS formation,which is an early indication of pro-inflammatory factor signaling.
Aim: Our previous data have shown that type II alveolar epithelial (AEII) cellsexpress neuropeptide calcitonin gene-related peptide (CGRP), and that pro-in-flammatory factor interleukin 1-β (IL- 1β) induces CGRP secretion in the A549 hu -man AEII cell line. in the present study, we investigated the effect of endogenousand exogenous CGRP on IL-1β-induced chemokine interleukin-8 (IL-8) secretion. Methods: We used enzyme-linked immunosorbent assay -PCR todetect IL-8 protein and mRNA levels, respectively, siRNA and the stably trans-fected cell line were used to knock down and overexpress the CGRP gene, respectively, and chemiluminescence assay was used to detect reactive oxygenspecies (ROS) formation. Results : CGRP-1 receptor antagonist hCGRP_ (8-37) (0.1-1nmol·L -1) greatly amplified IL-1β-induced IL-8 production.The inhibition of CGRPexpression by siRNA increased IL-8 secretion upon IL -1β stimulation. However, cell clones stably transfected with CGRP showed significantly inhibited ed mRNA and protein levels of IL-8 induced by 1L-1β.Conclusion: These data implythat AEII cell-derived CGRP suppress IL-1β-induced IL-8 secretion in an autocrine / paracrine mode.Further investigation showed that CGRP attenuated IL-1β -arousedROS formation, which is an early indication of pro-inflammatory factor signaling.