Oxysophocarpine protects airway epithelial cells against inflammation and apoptosis by inhibiting miR-155 expression

2020 ◽  
Vol 12 (16) ◽  
pp. 1475-1487
Author(s):  
Linfu Li ◽  
Renbing Shi ◽  
Weimei Shi ◽  
Rui Zhang ◽  
Longhuo Wu
Keyword(s):  
Epithelial Cells ◽  
Protein Interactions ◽  
Inflammatory Responses ◽  
Annexin V ◽  
Airway Epithelial Cells ◽  
Protective Effects ◽  
Airway Epithelial ◽  
Quantitative Real Time Pcr ◽  
Protein Expressions ◽  
Anti Inflammation

Oxysophocarpine (OSC) has been documented for anti-inflammatory activity. However, the mechanisms of OSC in anti-inflammation are unclear. Aim: To investigate the protective effects of OSC on inflammation and apoptosis induced by lipopolysaccharide in NCI-H292 and human primary airway epithelial cells. Materials & methods: MTT and Annexin V-FITC/PI staining were used to detect cells viability. Inflammatory responses were determined by ELISA. The quantitative real-time PCR (qRT-PCR) and western blot were used to detect mRNA/miRNA and protein expressions respectively. Co-immunoprecipitation was investigated for protein interactions. Results & conclusion: miR-155 mimics significantly induced cell apoptosis, inflammatory responses and MAPK and NF-κB pathways. NDFIP1 was identified as the target of miR-155. OSC protected cells against apoptosis and inflammatory responses and compromised miR-155 activity by attenuating MAPK and NF-κB pathways.

scholarly journals Overproduction of growth differentiation factor 15 promotes human rhinovirus infection and virus-induced inflammation in the lung

2018 ◽  
Vol 314 (3) ◽  
pp. L514-L527 ◽  
Author(s):  
Qun Wu ◽  
Di Jiang ◽  
Niccolette R. Schaefer ◽  
Laura Harmacek ◽  
Brian P. O’Connor ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Human Rhinovirus ◽  
Chronic Obstructive ◽  
Airway Epithelial ◽  
Growth Differentiation Factor 15 ◽  
Human Airway ◽  
Differentiation Factor ◽  
Human Airway Epithelial Cells

Human rhinovirus (HRV) is the most common virus contributing to acute exacerbations of chronic obstructive pulmonary disease (COPD) nearly year round, but the mechanisms have not been well elucidated. Recent clinical studies suggest that high levels of growth differentiation factor 15 (GDF15) protein in the blood are associated with an increased yearly rate of all-cause COPD exacerbations. Therefore, in the current study, we investigated whether GDF15 promotes HRV infection and virus-induced lung inflammation. We first examined the role of GDF15 in regulating host defense and HRV-induced inflammation using human GDF15 transgenic mice and cultured human GDF15 transgenic mouse tracheal epithelial cells. Next, we determined the effect of GDF15 on viral replication, antiviral responses, and inflammation in human airway epithelial cells with GDF15 knockdown and HRV infection. Finally, we explored the signaling pathways involved in airway epithelial responses to HRV infection in the context of GDF15. Human GDF15 protein overexpression in mice led to exaggerated inflammatory responses to HRV, increased infectious particle release, and decreased IFN-λ2/3 (IL-28A/B) mRNA expression in the lung. Moreover, GDF15 facilitated HRV replication and inflammation via inhibiting IFN-λ1/IL-29 protein production in human airway epithelial cells. Lastly, Smad1 cooperated with interferon regulatory factor 7 (IRF7) to regulate airway epithelial responses to HRV infection partly via GDF15 signaling. Our results reveal a novel function of GDF15 in promoting lung HRV infection and virus-induced inflammation, which may be a new mechanism for the increased susceptibility and severity of respiratory viral (i.e., HRV) infection in cigarette smoke-exposed airways with GDF15 overproduction.

Innate Inflammatory Responses of Pediatric Cystic Fibrosis Airway Epithelial Cells

2011 ◽  
Vol 44 (6) ◽  
pp. 761-767 ◽  
Author(s):  
Erika N. Sutanto ◽  
Anthony Kicic ◽  
Clara J. Foo ◽  
Paul T. Stevens ◽  
David Mullane ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Cystic Fibrosis Airway

scholarly journals Streamer discharge reduces pollen-induced inflammatory responses and injury in human airway epithelial cells

2013 ◽  
Vol 238 (2) ◽  
pp. 187-192
Author(s):  
Akiko Honda ◽  
Rumiko Murayama ◽  
Kenshi Tsuji ◽  
Yugo Matsuda ◽  
Eiko Koike ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Streamer Discharge ◽  
Human Airway ◽  
Human Airway Epithelial Cells

scholarly journals Cultured Human Airway Epithelial Cells (Calu-3): A Model of Human Respiratory Function, Structure, and Inflammatory Responses

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Yan Zhu ◽  
Aaron Chidekel ◽  
Thomas H. Shaffer
Keyword(s):  
Epithelial Cells ◽  
Cellular Response ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Treatment Modalities ◽  
Positive Pressure ◽  
Dependent Manner ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells

This article reviews the application of the human airway Calu-3 cell line as a respiratory model for studying the effects of gas concentrations, exposure time, biophysical stress, and biological agents on human airway epithelial cells. Calu-3 cells are grown to confluence at an air-liquid interface on permeable supports. To model human respiratory conditions and treatment modalities, monolayers are placed in an environmental chamber, and exposed to specific levels of oxygen or other therapeutic modalities such as positive pressure and medications to assess the effect of interventions on inflammatory mediators, immunologic proteins, and antibacterial outcomes. Monolayer integrity and permeability and cell histology and viability also measure cellular response to therapeutic interventions. Calu-3 cells exposed to graded oxygen concentrations demonstrate cell dysfunction and inflammation in a dose-dependent manner. Modeling positive airway pressure reveals that pressure may exert a greater injurious effect and cytokine response than oxygen. In experiments with pharmacological agents, Lucinactant is protective of Calu-3 cells compared with Beractant and control, and perfluorocarbons also protect against hyperoxia-induced airway epithelial cell injury. The Calu-3 cell preparation is a sensitive and efficient preclinical model to study human respiratory processes and diseases related to oxygen- and ventilator-induced lung injury.

Obese Adipose Tissue Modulates Pro-inflammatory Responses of Mouse Airway Epithelial Cells

2021 ◽  
Author(s):  
Jennifer L Ather ◽  
Katherine E Van Der Vliet ◽  
Madeleine M Mank ◽  
Leah F Reed ◽  
Anne E Dixon ◽  
...  
Keyword(s):  
Weight Loss ◽  
Epithelial Cells ◽  
High Fat Diet ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Obese Mice ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet

Although recognized as an important endocrine organ, little is known about the mechanisms through which adipose tissue can regulate inflammatory responses in distant tissues, such as lung, that are affected by obesity. To explore potential mechanisms, male C57BL/6J mice were provided either high-fat diet, low-fat diet, or were provided a high-fat diet then switched to the low-fat diet to promote weight loss. Visceral adipocytes were then cultured in vitro to generate conditioned media (CM) that was used to treat both primary (MTEC) and immortalized (MTCC) airway epithelial cells. Adiponectin levels were greatly depressed in the CM from both obese and diet-switched adipocytes relative to mice continually fed the low-fat diet. MTEC from obese mice secreted higher baseline levels of inflammatory cytokines than MTEC from lean or diet-switched mice. MTEC treated with obese adipocyte CM increased their secretion of these cytokines compared to MTEC treated with lean CM. Diet-switched CM modestly decreased the production of cytokines compared to obese CM, and these effects were recapitulated when the CM was used to treat MTCC. Adipose stromal vascular cells from obese mice expressed genes consistent with an M1 macrophage phenotype and decreased eosinophil abundance compared to lean SVF, a profile that persisted in the lean diet-switched mice despite substantial weight loss. Soluble factors secreted from obese adipocytes exert a pro-inflammatory effect on airway epithelial cells, and these alterations are attenuated by diet-induced weight loss, which could have implications for the airway dysfunction related to obese asthma and its mitigation by weight loss.

Mechanisms That Potentially Underlie Virus-Induced Exaggerated Inflammatory Responses By Airway Epithelial Cells

CHEST Journal ◽  
2003 ◽  
Vol 123 (3) ◽  
pp. 391S-392S
Author(s):  
René Lutter ◽  
Matthijs van Wissen ◽  
Thierry Roger ◽  
Paul Bresser ◽  
Koen van der Sluijs ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Airway Epithelial

scholarly journals Capsular Polysaccharide is a Main Component ofMycoplasma ovipneumoniaein the Pathogen-Induced Toll-Like Receptor-Mediated Inflammatory Responses in Sheep Airway Epithelial Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Zhongjia Jiang ◽  
Fuyang Song ◽  
Yanan Li ◽  
Di Xue ◽  
Guangcun Deng ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Capsular Polysaccharide ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Atypical Pneumonia ◽  
Activator Protein 1 ◽  
Airway Epithelial ◽  
Toll Like Receptor ◽  
Bronchial Epithelial

Mycoplasma ovipneumoniae(M. ovipneumoniae) is characterized as an etiological agent of primary atypical pneumonia that specifically infects sheep and goat. In an attempt to better understand the pathogen-host interaction between the invadingM. ovipneumoniaeand airway epithelial cells, we investigated the host inflammatory responses against capsular polysaccharide (designated as CPS) ofM. ovipneumoniaeusing sheep bronchial epithelial cells cultured in an air-liquid interface (ALI) model. Results showed that CPS derived fromM. ovipneumoniaecould activate toll-like receptor- (TLR-) mediated inflammatory responses, along with an elevated expression of nuclear factor kappa B (NF-κB), activator protein-1 (AP-1), and interferon regulatory factor 3 (IRF3) as well as various inflammatory-associated mediators, representatively including proinflammatory cytokines, such as IL1β, TNFα, and IL8, and anti-inflammatory cytokines such as IL10 and TGFβof TLR signaling cascade. Mechanistically, the CPS-induced inflammation was TLR initiated and was mediated by activations of both MyD88-dependent and MyD88-independent signaling pathways. Of importance, a blockage of CPS with specific antibody led a significant reduction ofM. ovipneumoniae-induced inflammatory responses in sheep bronchial epithelial cells. These results suggested that CPS is a key virulent component ofM. ovipneumoniae, which may play a crucial role in the inflammatory response induced byM. ovipneumoniaeinfections.

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