scholarly journals A Long Noncoding RNA Antisense to ICAM-1 Is Involved in Allergic Asthma Associated Hyperreactive Mucous Response of Airway Epithelial Cells

2020 ◽  
Author(s):  
D. Devadoss ◽  
G. Daly ◽  
M. Manevski ◽  
D. Houserova ◽  
S.S. Hussain ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Allergic Asthma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Airway Epithelial Cells ◽  
Airway Epithelial

scholarly journals Airway Epithelial Cells Are Crucial Targets of Glucocorticoids in a Mouse Model of Allergic Asthma

2017 ◽  
Vol 199 (1) ◽  
pp. 48-61 ◽  
Author(s):  
Carina Klaßen ◽  
Anna Karabinskaya ◽  
Lien Dejager ◽  
Sabine Vettorazzi ◽  
Justine Van Moorleghem ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mouse Model ◽  
Allergic Asthma ◽  
Airway Epithelial Cells ◽  
Airway Epithelial

scholarly journals Human Metapneumovirus Infection Induces Significant Changes in Small Noncoding RNA Expression in Airway Epithelial Cells

2014 ◽  
Vol 3 ◽  
pp. e163 ◽  
Author(s):  
Junfang Deng ◽  
Ryan N Ptashkin ◽  
Qingrong Wang ◽  
Guangliang Liu ◽  
Guanping Zhang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Noncoding Rna ◽  
Airway Epithelial Cells ◽  
Human Metapneumovirus ◽  
Rna Expression ◽  
Airway Epithelial ◽  
Small Noncoding Rna

scholarly journals Nrf2 reduces allergic asthma in mice through enhanced airway epithelial cytoprotective function

2015 ◽  
Vol 309 (1) ◽  
pp. L27-L36 ◽  
Author(s):  
Thomas E. Sussan ◽  
Sachin Gajghate ◽  
Samit Chatterjee ◽  
Pooja Mandke ◽  
Sarah McCormick ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Allergic Asthma ◽  
Airway Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Related Factor ◽  
Airway Epithelial ◽  
Zonula Occludens ◽  
Lung Epithelial ◽  
Zonula Occludens 1

Asthma development and pathogenesis are influenced by the interactions of airway epithelial cells and innate and adaptive immune cells in response to allergens. Oxidative stress is an important mediator of asthmatic phenotypes in these cell types. Nuclear erythroid 2-related factor 2 ( Nrf2) is a redox-sensitive transcription factor that is the key regulator of the response to oxidative and environmental stress. We previously demonstrated that Nrf2-deficient mice have heightened susceptibility to asthma, including elevated oxidative stress, inflammation, mucus, and airway hyperresponsiveness (AHR) (Rangasamy T, Guo J, Mitzner WA, Roman J, Singh A, Fryer AD, Yamamoto M, Kensler TW, Tuder RM, Georas SN, Biswal S. J Exp Med 202: 47–59, 2005). Here we dissected the role of Nrf2 in lung epithelial cells and tested whether genetic or pharmacological activation of Nrf2 reduces allergic asthma in mice. Cell-specific activation of Nrf2 in club cells of the airway epithelium significantly reduced allergen-induced AHR, inflammation, mucus, Th2 cytokine secretion, oxidative stress, and airway leakiness and increased airway levels of tight junction proteins zonula occludens-1 and E-cadherin. In isolated airway epithelial cells, Nrf2 enhanced epithelial barrier function and increased localization of zonula occludens-1 to the cell surface. Pharmacological activation of Nrf2 by 2-trifluoromethyl-2′-methoxychalone during the allergen challenge was sufficient to reduce allergic inflammation and AHR. New therapeutic options are needed for asthma, and this study demonstrates that activation of Nrf2 in lung epithelial cells is a novel potential therapeutic target to reduce asthma susceptibility.

Identification of histone acetylation in a murine model of allergic asthma by proteomic analysis

2020 ◽  
pp. 153537022098034
Author(s):  
Yuan Ren ◽  
Menglu Li ◽  
Shiyao Bai ◽  
Lingfei Kong ◽  
Xinming Su
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Smooth Muscle Cells ◽  
Histone Acetylation ◽  
Allergic Asthma ◽  
Inflammatory Cells ◽  
Muscle Cells ◽  
Airway Epithelial Cells ◽  
Whole Body ◽  
Airway Epithelial

The pathogenesis of asthma is closely related to histone acetylation modification, but the specific acetylation sites related to this process remain indistinct. Herein, our study sought to identify differentially modified acetylation sites and their expression distribution in cells involved in asthma in lung tissues. The airway hyper-responsiveness, inflammation, and remodeling were assessed by non-invasive whole-body plethysmography, ELISA, and hematoxylin-eosin staining to confirm the successful establishment of the allergic asthma model. Afterward, the differentially modified acetylation sites in asthmatic lung tissues were identified and validated by using proteomics and western blotting, respectively. The immunohistochemistry analysis was applied to reveal the distribution of identified acetylation sites in asthmatic lung tissues. A total of 15 differentially modified acetylation sites, including 13 upregulated (H3K9ac, H3K14ac, H3K18ac, H3K23ac,H3K27ac, H3K36ac, H2B1KK120ac, H2B2BK20ac, H2BK16ac, H2BK20ac, H2BK108ac, H2BK116ac, and H2BK120ac) and 2 downregulated (H2BK5ac and H2BK11ac) sites were identified and validated. Furthermore, immunohistochemical staining of lung tissues showed that nine of the identified histone acetylation sites (H2BK5, H2BK11, H3K18, H2BK116, H2BK20, H2BK120, H3K9, H3K36, and H3K27) were differentially expressed in airway epithelial cells, and the acetylation of identified H3 histones were observed in both eosinophil and perivascular inflammatory cells. Additionally, differential expression of histone acetylation sites was also observed in nucleus of airway epithelial cells, vascular smooth muscle cells, perivascular inflammatory cells, and airway smooth muscle cells. In conclusion, we identified potential acetylation sites associated with asthma pathogenesis. These findings may contribute greatly in the search for therapeutic approaches for allergic asthma.

Pro-inflammatory mediators increase levels of the noncoding RNA GAS5 in airway smooth muscle and epithelial cells

2015 ◽  
Vol 93 (3) ◽  
pp. 203-206 ◽  
Author(s):  
Christine R. Keenan ◽  
Michael J. Schuliga ◽  
Alastair G. Stewart
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Airway Smooth Muscle ◽  
Inflammatory Mediators ◽  
Noncoding Rna ◽  
Cell Types ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Structural Cell ◽  
Glucocorticoid Sensitivity

The long noncoding RNA (lncRNA) GAS5 has been found to act as a decoy for the glucocorticoid receptor (GR), thus implicating GAS5 as a potential regulator of glucocorticoid sensitivity and resistance. Airway smooth muscle (ASM) cells and airway epithelial cells (AEC) play an important role in the pathogenesis and persistence of asthma and other chronic airways diseases. These airway structural cell types are also important cellular targets of the anti-inflammatory actions of glucocorticoids. In this study, we sought to examine the relevance of GAS5 to glucocorticoid sensitivity and resistance in ASM and AEC. We provide the first evidence that pro-inflammatory mediators up-regulate GAS5 levels in both airway epithelial and smooth muscle cells, and that decreasing GAS5 levels can enhance glucocorticoid action in AEC.

scholarly journals Kaempferol Suppresses Eosionphil Infiltration and Airway Inflammation in Airway Epithelial Cells and in Mice with Allergic Asthma

2011 ◽  
Vol 142 (1) ◽  
pp. 47-56 ◽  
Author(s):  
Ju-Hyun Gong ◽  
Daekeun Shin ◽  
Seon-Young Han ◽  
Jung-Lye Kim ◽  
Young-Hee Kang
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Airway Epithelial Cells ◽  
Airway Epithelial

scholarly journals Attenuated lncRNA NKILA Enhances the Secretory Function of Airway Epithelial Cells Stimulated by Mycoplasma pneumoniae via NF-κB

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Fengxia Zhang ◽  
Jiamin Zhang ◽  
Feng Liu ◽  
Yao Zhou ◽  
Yun Guo ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mycoplasma Pneumoniae ◽  
Noncoding Rna ◽  
Nuclear Translocation ◽  
A549 Cells ◽  
Airway Epithelial Cells ◽  
Regulatory Function ◽  
Airway Epithelial ◽  
Secretory Function ◽  
Tnf Α

The secretory function of airway epithelial cells is important in the pathogenesis of Mycoplasma pneumoniae pneumonia (MPP). To investigate the regulatory function of NKILA (nuclear factor-κB (NF-κB) interacting long noncoding RNA (lncRNA)) in MPP, we first detected NKILA as well as the concentration of interleukin 8 (IL-8) and tumor necrosis factor-α (TNF-α) in bronchoalveolar lavage fluid of children with MPP. Then, NKILA was knocked down in epithelial cells to investigate its effect on their secretory function. The results suggested that NKILA was downregulated in children with MPP, while IL-8 and TNF-α levels increased. Knockdown of NKILA in vitro promoted the inflammatory effects of Mycoplasma pneumoniae (MP) in epithelial A549 and BEAS-2B cells. Knockdown of NKILA promoted inhibitor of κBα (IκBα) phosphorylation and degradation, and NF-κB p65 nuclear translocation. Furthermore, RNA immunoprecipitation showed that NKILA could physically bind to IκBα in MP-treated A549 cells. Collectively, our data demonstrated that attenuation of NKILA enhances the effects of MP-stimulated secretory functions of epithelial cells via regulation of NF-κB signaling.

Differentiation of human pluripotent stem cells into airway epithelial cells

Pneumologie ◽  
2015 ◽  
Vol 69 (07) ◽  
Author(s):  
S Ulrich ◽  
S Weinreich ◽  
R Haller ◽  
S Menke ◽  
R Olmer ◽  
...  
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
Pluripotent Stem Cells ◽  
Airway Epithelial Cells ◽  
Human Pluripotent Stem Cells ◽  
Airway Epithelial
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