Open AccessCalcitonin gene‐related peptide inhibits interleukin‐1 β‐induced interleukin‐8 secretion in human type II alveolar epithelial cells 1
Author(s) -
LI Wenjing,
WANG Tengke,
WANG Xian
Publication year - 2006
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2006.00408.x
Subject(s) - calcitonin gene related peptide , secretion , transfection , autocrine signalling , interleukin 8 , calcitonin , medicine , endocrinology , receptor , cell culture , interleukin , chemistry , paracrine signalling , microbiology and biotechnology , cytokine , biology , neuropeptide , genetics
Aim : Our previous data have shown that type II alveolar epithelial (AEII) cells express neuropeptide calcitonin gene‐related peptide (CGRP), and that pro‐inflammatory factor interleukin1‐β (IL‐1β) induces CGRP secretion in the A549 human AEII cell line. In the present study, we investigated the effect of endogenous and exogenous CGRP on IL‐1β‐induced chemokine interleukin‐8 (IL‐8) secretion. Methods : We used enzyme‐linked immunosorbent assay (ELISA) and RT‐PCRto detect 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 oxygen species (ROS) formation. Results : CGRP‐1 receptor antagonist hCGRP 8–37 (0.1–1 nmol‐L −1 ) greatly amplified IL‐1 β‐induced IL‐8 production. The inhibition of CGRP expression by siRNA significantly increased IL‐8 secretion upon IL‐1β stimulation. However, cell clones stably transfected with CGRP showed significantly inhibited mRNAandproteinlevelsofIL‐8 inducedbyIL‐1β. Conclusion : These data imply that AEII cell‐derived CGRP suppress IL‐1 β‐induced IL‐8 secretion in an autocrine/paracrine mode. Further investigation showed that CGRP attenuated IL‐1 β‐aroused ROS formation, which is an early indication of pro‐inflammatory factor signaling.