Lipopolysaccharide-induced CCN1 production enhances interleukin-6 secretion in bronchial epithelial cells

Shi, Lin; Dong, Nian; Ji, Dongxiang; Huang, Xiaomin; Ying, Zhaojian; Wang, Xiangdong; Chen, Chengshui

doi:10.1007/s10565-017-9401-1

Cited by 36 publications

(25 citation statements)

References 31 publications

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“…53 Airway epithelial cells are involved in the secretion of several molecules as surfactant components and pro-inflammatory mediators. 54,55 Interleukin 6 (IL-6) and Interleukin 8 (IL-8) are strongly involved in respiratory acute lung injury. Pires-Neto et al showed that airway epithelial cells from patients with ARDS have increased expression of IL-8 and IL-6 compared with controls.…”

Section: Covid-19mentioning

confidence: 99%

SARS‐CoV‐2 and the possible connection to ERs, ACE2, and RAGE: Focus on susceptibility factors

et al. 2020

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has provoked major stresses on the health-care systems of several countries, and caused the death of more than a quarter of a million people globally, mainly in the elderly population with preexisting pathologies. Previous studies with coronavirus (SARS-CoV) point to gender differences in infection and disease progression with increased susceptibility in male patients, indicating that estrogens may be associated with physiological protection against the coronavirus. Therefore, the objectives of this work are threefold. First, we aim to summarize the SARS-CoV-2 infection pathway and the roles both the virus and patient play in COVID-19 (Coronavirus disease 2019) progression, clinical symptomatology, and mortality. Second, we detail the effect estrogen has on viral infection and host infection response, including its role in both the regulation of key viral receptor expression and the mediation of inflammatory activity. Finally, we describe how ERs (estrogen receptors) and RAGE (receptor for advanced glycation end-products) play a critical role in metabolic pathways, which we 14104 | STILHANO eT AL. 1 | INTRODUCTION 1.1 | SARS-CoV-2 and COVID-19 Coronavirus disease 2019 (COVID-19) is a disease caused by the new coronavirus called SARS-CoV-2 (SARScoronavirus 2). In December 2019, the first case of COVID-19 was diagnosed in the city of Wuhan, China. 1 The virus disseminated rapidly and the World Health Organization (WHO) declared SARS-CoV-2 as a pandemic on March 11th 2020, given that it had already spread to more than 188 countries on five continents. Updated epidemiological data from the Johns Hopkins University indicator shows that there are more than 20 million cases and over 730 thousand deaths due to COVID-19 by the beginning of August 2020 (https://coron avirus.jhu.edu/map.html-accessed on August 11, 2020 14:00 GMT). The Case Fatality Rate (CFR) for COVID-19 increases exponentially with age. 2,3 For example, for patients aged between 65 and 74 years old, the CFR is 3%-5%, 4%-11% CFR for 75 and 84 years old and 10%-27% CFR for the patients above 85 years old. 2 Obesity, diabetes, and hypertension are comorbidities associated with increased risk for developing the severe form of COVID-19. Data attributed to the Centers for Disease Control and Prevention (https://www.cdc.gov/coron aviru s/2019-ncov/need-extra preca ution s/group sat -highe r-risk. html) shows that diabetes is one of the major risk factors for fatal outcomes from COVID-19. Considering that diabetic patients usually have hyperglycemia, impaired immune function, and several comorbidities such as hypertension, dyslipidemia, and cardiovascular disease, this group is more susceptible to be severely infected by SARS-CoV-2. 4 Another important risk for fatal COVID-19 is obesity, particularly in males. 5,6 Moreover, COVID-19 also affects more severely individuals with metabolic syndrome, probably because these patients have a pro-inflammatory condition that may contribute to enhance...

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Section: Covid-19mentioning

confidence: 99%

SARS‐CoV‐2 and the possible connection to ERs, ACE2, and RAGE: Focus on susceptibility factors

et al. 2020

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“…The expression levels of inflammatory genes were measured in the presence of the Hh agonist (SAG) and antagonist (Cyclo). The responsiveness of DC2 cells to the inflammatory condition was first assessed by examining the expression level of interleukin‐6 (IL‐6), an LPS mediated‐inflammation factor 31,32 . After a 6‐hour treatment with LPS, IL‐6 expression was upregulated 2‐fold (Figure 5A), confirming DC2 responsiveness to the inflammatory condition.…”

Section: Resultsmentioning

confidence: 85%

Hedgehog signaling pathway regulates gene expression profile of epididymal principal cells through the primary cilium

et al. 2020

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Primary cilia (PC) are organelles that sense and respond to dynamic changes of the extracellular milieu through the regulation of target genes. By using the epididymis as a model system, we determined the contribution of primary cilia in the regulation of epithelial cell functions through the transduction of the Hedgehog (Hh) signaling pathway. Both Sonic (SHH) and Indian Hedgehog (IHH) ligands were detected in epididymal epithelial cells by confocal microscopy and found secreted in the extracellular space. Gene expression profiling preformed on ciliated epithelial cells indicated that 153 and 1052 genes were differentially expressed following treatment with the Hh agonist SAG or the Hh antagonist cyclopamine (Cyclo), respectively. Strikingly, gene ontology analysis indicated that genes associated with immune response were the most affected following Hh modulation. The contribution of epididymal PC to canonical Hh pathway transduction was validated by ciliobrevin D treatment, which induced a significant decrease in PC length and a reduction in the expression Hh signaling targets. Such findings bring us closer to a molecular understanding of the subtle immune balance observed in some epithelia, including the epididymis and the intestine, which are organs featuring both tolerance toward autoimmune spermatozoa (or commensal bacteria) and defense against pathogens.

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“…A previous study has shown that A549 cells release IL-1β and TNF-α after LPS stimulation though autocrine modes (36). This exerts a strong and synergic induction signal for IL-6 (37), since a high increase of IL-6 in ALI/ARDS accelerates the development of the local inflammatory microenvironment (38). Moreover, high levels of IL-1β, IL-6 and TNF-α have been considered as the most promising biomarkers for predicting morbidity and mortality in patients with ALI/ARDS (39).…”

Section: Discussionmentioning

confidence: 97%

Regulatory mechanism of NOV/CCN3 in the inflammation and apoptosis of lung epithelial alveolar cells upon lipopolysaccharide stimulation

Zhu

Huang

et al. 2019

Mol Med Report

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Lipopolysaccharide (LPS) induces inflammatory stress and apoptosis. Pulmonary epithelial cell apoptosis has been shown to accelerate the progression of acute lung injury (ali)/acute respiratory distress syndrome (ARDS), and is the leading cause of mortality in patients with ALI/ARDS. Nephroblastoma overexpressed (NOV; also known as CCN3), an inflammatory modulator, is reported to be a biomarker in ALI. Using an LPS-induced ALI model, we investigated the expression of CCN3 and its possible molecular mechanism involved in lung alveolar epithelial cell inflammation and apoptosis. Our data revealed that LPS treatment greatly increased the level of CCN3 in human lung alveolar type II epithelial cells (A549 cell line). The A549 cells were also transfected with a specific CCN3 small interfering RNA (siRNA). CCN3 knockdown not only largely attenuated the expression of inflammatory cytokines, interleukin (IL)-1β and transforming growth factor (TGF)-β1, but also reduced the apoptotic rate of the A549 cells and altered the expression of apoptosis-associated proteins (Bcl-2 and caspase-3). Furthermore, CCN3 knockdown greatly inhibited the activation of nuclear factor (NF)-κB p65 in the A549 cells, and TGF-β/p-Smad and NF-κB inhibitors significantly decreased the expression level of CCN3 in A549 cells. In conclusion, our data indicate that CCN3 knockdown affects the expression of downstream genes through the TGF-β/p-Smad or NF-κB pathways, leading to the inhibition of cell inflammation and apoptosis in human alveolar epithelial cells.

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Lipopolysaccharide-induced CCN1 production enhances interleukin-6 secretion in bronchial epithelial cells

Cited by 36 publications

References 31 publications

SARS‐CoV‐2 and the possible connection to ERs, ACE2, and RAGE: Focus on susceptibility factors

SARS‐CoV‐2 and the possible connection to ERs, ACE2, and RAGE: Focus on susceptibility factors

Hedgehog signaling pathway regulates gene expression profile of epididymal principal cells through the primary cilium

Regulatory mechanism of NOV/CCN3 in the inflammation and apoptosis of lung epithelial alveolar cells upon lipopolysaccharide stimulation

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