Dataset Information

Cigarette Smoke Extract Enhances IL-17A-Induced IL-8 Production via Up-Regulation of IL-17R in Human Bronchial Epithelial Cells.

ABSTRACT: Interleukin-17A (IL-17A) is a pro-inflammatory cytokine mainly derived from T helper 17 cells and is known to be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) has been considered as a primary risk factor of COPD. However, the interaction between CS and IL-17A and the underlying molecular mechanisms have not been clarified. In the current study, we investigated the effects of cigarette smoke extract (CSE) on IL-17A-induced IL-8 production in human bronchial epithelial cells, and sought to identify the underlying molecular mechanisms. IL-8 production was significantly enhanced following treatment with both IL-17A and CSE, while treatment with either IL-17A or CSE alone caused only a slight increase in IL-8 production. CSE increased the transcription of IL-17RA/RC and surface membrane expression of IL-17R, which was suppressed by an inhibitor of the phosphoinositide 3-kinase (PI3K)/Akt pathway (LY294002). CSE caused inactivation of glycogen synthase kinase-3? (GSK-3?) via the PI3K/Akt pathway. Blockade of GSK-3? inactivation by overexpression of constitutively active GSK-3? (S9A) completely suppressed the CSE-induced up-regulation of IL-17R expression and the CSE-induced enhancement of IL-8 secretion. In conclusion, inactivation of GSK-3? via the PI3K/Akt pathway mediates CSE-induced up-regulation of IL-17R, which contributes to the enhancement of IL-17A-induced IL-8 production.

SUBMITTER: Lee KH

PROVIDER: S-EPMC5935094 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature

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Cigarette Smoke Extract Enhances IL-17A-Induced IL-8 Production via Up-Regulation of IL-17R in Human Bronchial Epithelial Cells.

Lee Kyoung-Hee KH Lee Chang-Hoon CH Woo Jisu J Jeong Jiyeong J Jang An-Hee AH Yoo Chul-Gyu CG

Molecules and cells 20180221 4

Interleukin-17A (IL-17A) is a pro-inflammatory cytokine mainly derived from T helper 17 cells and is known to be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) has been considered as a primary risk factor of COPD. However, the interaction between CS and IL-17A and the underlying molecular mechanisms have not been clarified. In the current study, we investigated the effects of cigarette smoke extract (CSE) on IL-17A-induced IL-8 production in hu ...[more]

PMID: 29463070

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Project description:IntroductionThis study aimed to elucidate the biological implication of miR-937 in cigarette smoke extract (CSE)-induced human bronchial epithelial (HBE) cells and to further investigate its possible regulatory mechanism.MethodsPublic datasets were downloaded to identify differentially expressed genes and subjected to Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis in chronic obstructive pulmonary disease (COPD). Online prediction site and luciferase reporter assay were applied to determine the target correlation between miR-937 and IL1B. RT-qPCR, Western blot and Enzyme-Linked Immunosorbent Assays (ELISA) analyses were used to evaluate the expressions of indicated molecules. HBE cells were exposed with CSE (20 μg/mL) to construct the in vitro COPD model. Cell proliferation and apoptosis were measured through cell counting kit 8 and Annexin-V/propidium iodide (PI) staining assays.ResultsIL1B was found to be up-regulated in COPD samples compared with healthy controls and had a high correlation with the TNF and IL-17 pathways according to the data from GSE57148. Moreover, IL1B was predicted to be a target of miR-937, and it was negatively regulated by miR-937. CSE treatment reduced the miR-937 expression, meanwhile decreased the HBE cells proliferation, enhanced cells apoptosis, and elevated the expression of IL-6, IL-17, and TNF-α. Moreover, in the CSE model, upregulation of miR-937 promoted cells viability, restrained cells apoptosis, and decreased levels of IL-6, IL-17, and TNF-α were noted, which could be abolished by overexpression IL1B. In contrast, inhibiting miR-937 impeded cells proliferation, promoted cells apoptosis and elevated levels of IL-6, IL-17 and TNF-α, which could be rescued by IL1B-knockdown in CSE-induced HBEs.ConclusionsThese findings suggest that miR-937 plays a protective role on the HBEs after CSE damage, which may be achieved via targeting IL1B and inhibiting the TNF-α/IL-17 signaling pathway.

Dataset Information

Cigarette Smoke Extract Enhances IL-17A-Induced IL-8 Production via Up-Regulation of IL-17R in Human Bronchial Epithelial Cells.

Publications

Cigarette Smoke Extract Enhances IL-17A-Induced IL-8 Production via Up-Regulation of IL-17R in Human Bronchial Epithelial Cells.

Similar Datasets

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