A large lung gene expression study identifying IL1B as a novel player in airway inflammation in COPD airway epithelial cells

Gao, Yi; Liang, Min; Li, Ming; Fang, Xiangming; Liu, Jifang; Lai, Yuxiong; Chen, Jitao; Yao, Wenqian; Feng, Xiao; Hu, La; Chen, Lin; Zhou, Xinke; Liu, Zhaoyu

doi:10.1007/s00011-018-1145-8

Cited by 64 publications

(58 citation statements)

References 38 publications

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“…Chronic inflammation results from the inability of the body to resolve an acute inflammatory response. Persistent inflammation can trigger the development of various tumors such as colorectal cancer, gastric cancer, mucosa-associated lymphoid tissue cancer, lung cancer, bladder cancer, and HCC [200,201,202]. Hepatic inflammation for example as induced by hepatitis C virus infection is a cytokine driven disease, especially via IL-1β, triggering the transition from non-alcoholic fatty liver disease to severe fibrogenesis, and finally hepatocellular carcinoma [203].…”

Section: Role Of Il-1β In Tumor Developmentmentioning

confidence: 99%

“…Another significant mechanistic link between IL-1β and an increased risk of gastric cancer is the induction of aberrant DNA methylation via this interleukin [207]. IL-1β is also about 2–3-fold upregulated in small airway epithelial cells of chronic obstructive pulmonary disease (COPD) patients and seems to influence COPD airway inflammation [202]. Because COPD is a known risk factor for developing lung cancer [208], IL-1β seems to play a profound role in this regard as well.…”

Section: Role Of Il-1β In Tumor Developmentmentioning

confidence: 99%

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Interleukin-1 Beta—A Friend or Foe in Malignancies?

Bent

Moll

Grabbe

et al. 2018

IJMS

319

221

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Interleukin-1 beta (IL-1β) is induced by inflammatory signals in a broad number of immune cell types. IL-1β (and IL-18) are the only cytokines which are processed by caspase-1 after inflammasome-mediated activation. This review aims to summarize current knowledge about parameters of regulation of IL-1β expression and its multi-facetted role in pathophysiological conditions. IL-1 signaling activates innate immune cells including antigen presenting cells, and drives polarization of CD4+ T cells towards T helper type (Th) 1 and Th17 cells. Therefore, IL-1β has been attributed a largely beneficial role in resolving acute inflammations, and by initiating adaptive anti-tumor responses. However, IL-1β generated in the course of chronic inflammation supports tumor development. Furthermore, IL-1β generated within the tumor microenvironment predominantly by tumor-infiltrating macrophages promotes tumor growth and metastasis via different mechanisms. These include the expression of IL-1 targets which promote neoangiogenesis and of soluble mediators in cancer-associated fibroblasts that evoke antiapoptotic signaling in tumor cells. Moreover, IL-1 promotes the propagation of myeloid-derived suppressor cells. Using genetic mouse models as well as agents for pharmacological inhibition of IL-1 signaling therapeutically applied for treatment of IL-1 associated autoimmune diseases indicate that IL-1β is a driver of tumor induction and development.

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Section: Role Of Il-1β In Tumor Developmentmentioning

confidence: 99%

Section: Role Of Il-1β In Tumor Developmentmentioning

confidence: 99%

Interleukin-1 Beta—A Friend or Foe in Malignancies?

Bent

Moll

Grabbe

et al. 2018

IJMS

319

221

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“…And then the data were analysed with the Limma package in the R. The Limma package was designed for examining DEGs. 19 2.4 | Gene ontology and pathway enrichment analysis of DEGs Gene ontology (GO) analysis, a common useful method for highthroughput genome or transcriptome data, was used to identify characteristic biological function of DEGs. 23 The volcano plot and heat map of the DEGs were drawn via Heatmap and ggplot2 packages in R software.…”

Section: Degs Identificationmentioning

confidence: 99%

“…19 In the present study, we used three high-throughput microarray profiles to screen differentially expressed genes (DEGs) between OA and HC (DEGsOA) and RA and HC (DEGsRA). 19 In the present study, we used three high-throughput microarray profiles to screen differentially expressed genes (DEGs) between OA and HC (DEGsOA) and RA and HC (DEGsRA).…”

mentioning

confidence: 99%

Comparison of rheumatoid arthritis (RA) and osteoarthritis (OA) based on microarray profiles of human joint fibroblast‐like synoviocytes

Cai

Jiang

et al. 2018

Cell Biochemistry & Function

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The purpose of the present study was to investigate the underlying molecular mechanism of osteoarthritis (OA) and rheumatoid arthritis (RA) based on microarray profiles. Three human joint fibroblast-like synoviocytes (FLSs) microarray profiles including 26 OA samples, 33 RA samples, and 20 healthy control (HC) samples were downloaded from the GEO database. Differentially expressed genes (DEGs) between OA and HC (DEGsOA) and RA and HC (DEGsRA) were identified. Co-expressed and specific genes were analysed between DEGsOA and DEGsRA. Gene ontology, KEGG pathway enrichment, PPI network, and GSEA were performed to predict the function of DEGs. Two hundred seventy-six and 410 differential genes in DEGsOA and DEGsRA were observed. One hundred fifty coexpressed genes and 126 OA-specific genes (SELE, SERPINE1, and NFKBIA were the key genes) between DEGsOA and DEGsRA were enriched in the tumour necrosis factor (TNF) signalling pathway. However, 260 RA-specific genes of which the key genes were CCR5, CCR7, CXCR4, CCL5, and CCR4 were enriched in chemokine signalling pathway. Therefore, FLSs might exert an inflammatory effect by regulating TNF signalling pathway, targeting SELE, SERPINE1, and NFKBIA during the process of OA. Although TNF signalling pathway was also involved in the synovitis of RA, chemokine signalling pathway played the key role in RA FLSs mediating cell migration, invasion, and release of chemotaxis. In addition, CCR5, CCR7, CXCR4, CCL5, and CCR4 might be hub genes in RA. The different biomarkers and pathways identified in OA and RA may provide references for further study.List of abbreviations: CCL5, C-C motif chemokine ligand 5; CCRs, C-C motif chemokine receptors; CD95, FAS cell surface death receptor; Co-expressed genes, the common genes both in DEGsOA and DEGsRA groups; CXCR4, C-X-C motif chemokine receptor 4; DAVID, Database for Annotation, Visualization, and Integrated Discovery; DEGs, differently expressed genes; DEGsOA, differently expressed genes between osteoarthritis and healthy fibroblast-like synoviocytes; DEGsRA, differently expressed genes between rheumatoid arthritis and healthy fibroblast-like synoviocytes; DLL1, delta-like protein 1

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“…However, the role of the NLRP3 inflammasome in cigarette smoke-related diseases is still a matter of debate and available data are limited. [11][12][13] However, there is very limited evidence on the impact of cigarette smoke on the NLRP3 inflammasome in macrophages. [8][9][10] With respect to the NLRP3 inflammasome, growing evidence suggests that cigarette smoke activates the NLRP3 inflammasome in the lung epithelium, with increased expression of NLRP3, pro-IL-1β and caspase-1, higher caspase-1 activity and increased release of inflammasome-related cytokines IL-1β and IL-18.…”

mentioning

confidence: 99%

Cigarette smoke inhibits the NLRP3 inflammasome and leads to caspase‐1 activation via the TLR4‐TRIF‐caspase‐8 axis in human macrophages

et al. 2019

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The NLRP3 inflammasome is formed by the sensor NLRP3, the adaptor ASC, and pro‐caspase‐1. Assembly and activation of the inflammasome trigger caspase‐1‐dependent cleavage of pro‐IL‐1β and pro‐IL‐18 into their secreted forms. Cigarette smoke is a risk factor for chronic inflammatory diseases and is associated with macrophage dysfunction. The impact of cigarette smoke on NLRP3‐dependent responses in macrophages is largely unknown. Herein, we investigated the effects of cigarette smoke extract (CSE) on the NLRP3 inflammasome in human monocyte‐derived macrophages (MDMs) and THP‐1 cells stimulated with lipopolysaccharide (LPS) and LPS plus the NLRP3 inflammasome activator ATP. We found that CSE inhibited the release of IL‐1β and IL‐18 as well as the expression of NLRP3 acting mainly at the transcriptional level. Interestingly, we found that CSE increased the caspase‐1 activity via an NLRP3‐independent and TLR4‐TRIF‐caspase‐8‐dependent pathway. Activation of caspase‐1 by CSE led to a reduction of the basal glycolytic flux and impaired glycolytic burst in response to LPS. Overall, our findings unveil novel pathways leading to immune‐metabolic alterations in human macrophages exposed to cigarette smoke. These mechanisms may contribute to macrophage dysfunction and increased risk of infection in smokers.

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A large lung gene expression study identifying IL1B as a novel player in airway inflammation in COPD airway epithelial cells

Abstract: We identified IL1B was significantly up-regulated in COPD small airway epithelial cells and propose IL1B as a novel player in airway inflammation in COPD.

Cited by 64 publications

References 38 publications

Interleukin-1 Beta—A Friend or Foe in Malignancies?

Interleukin-1 Beta—A Friend or Foe in Malignancies?

Comparison of rheumatoid arthritis (RA) and osteoarthritis (OA) based on microarray profiles of human joint fibroblast‐like synoviocytes

Cigarette smoke inhibits the NLRP3 inflammasome and leads to caspase‐1 activation via the TLR4‐TRIF‐caspase‐8 axis in human macrophages

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