scholarly journals Regulatory Effects of Nur77 on Airway Remodeling and ASMC Proliferation in House Dust Mite-Induced Asthma

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Kun Wang ◽  
Muyun Wang ◽  
Yan Shang ◽  
Yanan He ◽  
Qiang Li ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Lung Diseases ◽  
Airway Remodeling ◽  
Vital Role ◽  
Cell Hyperplasia ◽  
Asthma Model ◽  
Dust Mite ◽  
Asthma Patients ◽  
Antioxidant Gene Expression ◽  
Regulatory Effects

Airway remodeling played a vital role in the development of asthma, and airway smooth muscle (ASM) mass was its hallmark. However, few strategies targeting ASM remodeling were developed in treating asthma. Nur77 was the transcription factor nuclear receptor involved in the pathogenesis of several lung diseases. Nur77 distribution and expression were determined in an HDM-mediated allergic asthma model. Its effect on airway hyperresponsiveness (AHR), chronic inflammation, and ASM remodeling in asthmatic mice was evaluated using a lentivirus-mediated shRNA. Possible mechanisms were explored by examining Nur77 actions and its underlying pathways in primary human AMC cells (ASMCs). In this study, we reported that Nur77 expression was mainly distributed along ASM and increased in lungs of HDM-challenged mice. Nur77 depletion by lentivirus-mediated shRNA ameliorated AHR, chronic inflammation, goblet cell hyperplasia, and airway remodeling in the asthmatic mouse model. By means of primary human ASMC, we discovered that Nur77 upregulation by HDM stimulation promoted cell proliferation and ROS production, as well as reduced antioxidant gene expression. These alterations might associate with MFN2/MAPK/AKT pathways. These findings broadened our understanding of airway remodeling and ASMC proliferation, which might provide a novel therapeutic target for asthma patients.

Prevention and Management of Respiratory Diseases Including Lung Cancer Through Exercise Interventions

2018 ◽  
Vol 3 (6) ◽  
Keyword(s):  
Chronic Inflammation ◽  
Respiratory Diseases ◽  
Disease Process ◽  
Chronic Obstructive Lung Disease ◽  
Chronic Obstructive ◽  
Pathological Feature ◽  
Cell Hyperplasia ◽  
Exercise Interventions ◽  
Asthma Patients ◽  
Potential Risk Factors

The objective of the paper is to create awareness among people about alternative and complimentary methods to protect themselves from respiratory diseases like asthma, bronchitis, chronic obstructive lung disease, cancer etc. The following changes take place in airways as a result of Lung diseases 1) Inflammation: Is a physiological process and plays the role of immunological defense against infection, injury or allergy 2) Hyper secretion of mucus: is a major pathological feature of Airway diseases. It is the result of goblet cell hyperplasia in respiratory mucosa and is a prominent feature of inflammation. Acute inflammation is a defense process and where as Chronic inflammation is a disease process. Chronic Inflammation and mucus hyper secretion are a potential risk factors for an accelerated loss of lung function. It is a common feature in elderly.. The thick viscous mucus in the Lungs will be conducive to pathogens. Continued inflammation and mucus hyper Secretion may significantly contribute to transformation of normal cells into cancer cells ( often as a result of chemical , viral or radioactive damage to genes) 3) Broncospasm: is an additional factor in asthma patients. The three factors together cause breathlessness.

Blockade of the NLRP3/Caspase-1 Axis Ameliorates Airway Neutrophilic Inflammation in a Toluene Diisocyanate-Induced Murine Asthma Model

2019 ◽  
Vol 170 (2) ◽  
pp. 462-475 ◽  
Author(s):  
Shuyu Chen ◽  
Lihong Yao ◽  
Peikai Huang ◽  
Qiaoling He ◽  
Hongbing Guan ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Airway Remodeling ◽  
Lavage Fluid ◽  
Vital Role ◽  
Toluene Diisocyanate ◽  
Receptor Protein ◽  
Th2 Response ◽  
Caspase 1 ◽  
Asthma Model

Abstract Multiple studies have addressed the vital role of Nod-like receptor protein 3(NLRP3)/caspase-1/IL-1β signaling in asthma. Yet, the role of NLRP3/caspase-1 in toluene diisocyanate (TDI)-induced asthma is still obscure. The aim of this study is to investigate the role of the NLRP3/caspase-1 axis in TDI-induced asthma. Using an established murine model of TDI-induced asthma as described previously, we gave the asthmatic mice a highly selective NLRP3 inhibitor, MCC950, as well as the specific caspase-1 inhibitors VX-765 and Ac-YVAD-CHO for therapeutic purposes. Airway resistance was measured and bronchoalveolar lavage fluid was analyzed. Lungs were examined by histology, immunohistochemistry, Western blotting, and flow cytometry. TDI exposure elevated the expression of NLRP3 and caspase-1 that was coupled with increased airway hyperresponsiveness (AHR), neutrophil-dominated cell infiltration, pronounced goblet cell metaplasia, extensive collagen deposition, and increased TH2/TH17 responses. Both VX-765 and Ac-YVAD-CHO effectively inhibited the activation of caspase-1 in TDI-asthmatic mice that was accompanied by dramatic attenuation of AHR, airway inflammation, and airway remodeling, in addition to a decreased TH2 response and lower levels of IL-18 and IL-1β. MCC950 blocked the activation of NLRP3 and downregulated protein expression of caspase-1, IL-1β, and IL-18 in TDI-exposed mice. Furthermore, MCC950 remarkably alleviated AHR, airway inflammation, airway remodeling, and significantly suppressed TH2/TH17 responses. These findings suggested that blockade of the NLRP3/caspase-1 axis effectively prevents the progression of TDI-induced asthma and could be used as therapeutic targets for asthmatics.

scholarly journals Effect of Low-Level Laser Therapy (LLLT) in Pulmonary Inflammation in Asthma Induced by House Dust Mite (HDM): Dosimetry Study

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Nicole Cristine Rigonato-Oliveira ◽  
Auriléia Aparecida de Brito ◽  
Luana Beatriz Vitoretti ◽  
Gabriel de Cunha Moraes ◽  
Tawany Gonçalves ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Laser Therapy ◽  
House Dust ◽  
House Dust Mite ◽  
Structural Parameters ◽  
Pulmonary Inflammation ◽  
Low Level Laser Therapy ◽  
Low Level Laser ◽  
Level Laser ◽  
Dust Mite

Asthma is characterized by chronic inflammation in the airways. Several models have been proposed for the discovery of new therapies. Low-Level Laser Therapy (LLLT) is relatively new and effective, very low cost, with no side effects. However, there is still no consensus on the optimal dose to be used. In this sense, the objective of the present study was to evaluate the best dose in an experimental model of asthma induced by House Dust Mite (HDM). Balb/c mice received administration of 100 ug/animal HDM and LLLT applications (diode laser: 660 nm, 100 mW and four different energies 1J, 3J, 5J, and 7.5J) for 16 days. After 24 hours, we studied inflammatory, functional, and structural parameters. The results showed that LBI was able to modulate the pulmonary inflammation observed by reducing the number of cells in Bronchoalveolar Lavage Fluid (BALF) as well as reducing the percentage of neutrophils, eosinophils and T lymphocytes. On the other hand, LLLT increased the level of IL-10 and reduced levels of IL-4, IL-5 and IL-13 in BALF. LLLT was able to reduce the production of mucus, peribronchial eosinophils, collagen deposition, bronchoconstriction index, and bronchial and muscular thickening in the airways. We concluded that the use of LLLT in the treatment of chronic inflammation of the airways attenuated the inflammatory process and functional and structural parameters. We emphasize, in general, that the 1J and 3J laser presented better results. Thus, photobiomodulation may be considered a promising tool for the treatment of chronic pulmonary allergic inflammation observed in asthma.

scholarly journals Effects of sublingual immunotherapy in a murine asthma model sensitized by intranasal administration of house dust mite extracts

2017 ◽  
Vol 66 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Kenjiro Shima ◽  
Toshiyuki Koya ◽  
Keisuke Tsukioka ◽  
Takuro Sakagami ◽  
Takashi Hasegawa ◽  
...  
Keyword(s):  
House Dust ◽  
House Dust Mite ◽  
Intranasal Administration ◽  
Sublingual Immunotherapy ◽  
Asthma Model ◽  
Dust Mite ◽  
Murine Asthma Model

Cytology of Nonneoplastic Occupational and Environmental Diseases of the Lung and Pleura

2007 ◽  
Vol 131 (11) ◽  
pp. 1700-1708 ◽  
Author(s):  
Rodolfo Laucirica ◽  
Mary L. Ostrowski
Keyword(s):  
Respiratory Tract ◽  
Lung Diseases ◽  
Asbestos Exposure ◽  
Cell Hyperplasia ◽  
Cytologic Examination ◽  
Diagnostic Categories ◽  
Etiologic Agents ◽  
Limited Experience ◽  
Occupational Lung Diseases

Abstract Context.—Cytologic examination of the respiratory tract has been a useful diagnostic tool when evaluating neoplastic lesions of the respiratory tract. However, we have limited experience in the application of this technique in the management of nonneoplastic occupational and environmental diseases of the lung and pleura. This review focuses on the cytologic characteristics of a variety of occupational lung diseases, grouping them into 2 broad diagnostic categories: reactive cellular changes and noncellular elements. The former includes entities such as reactive mesothelial proliferation, goblet cell metaplasia, Creola bodies, and reserve cell hyperplasia, and the latter encompasses Curschmann spirals, Charcot-Leyden crystals, and asbestos bodies. Objective.—To illustrate the cytologic features of several nonneoplastic occupational and environmental diseases and correlate the cytology with various etiologic agents. Data Sources.—Case-derived material and literature review. Conclusions.—The role of cytology in the diagnosis of nonneoplastic occupational and environmental lung diseases is limited. This may be because more than one agent can elicit a similar host reaction and/or the offending agent can be associated with more than one pathologic process. However, in the appropriate clinical and radiographic setting, the cytology can render valuable diagnostic information. Examples include pulmonary alveolar proteinosis in patients with acute silicoproteinosis and asbestos bodies in bronchoalveolar lavage samples of patients with asbestos exposure.

Inhibition of airway remodeling and inflammation by isoforskolin in PDGF-induced rat ASMCs and OVA-induced rat asthma model

2017 ◽  
Vol 95 ◽  
pp. 275-286 ◽  
Author(s):  
Xin Liang ◽  
Jingjing Wang ◽  
Weiwei Chen ◽  
Xiaoying Ma ◽  
Yaqin Wang ◽  
...  
Keyword(s):  
Airway Remodeling ◽  
Asthma Model

Regulation of the IL-33/ST2 Pathway Contributes to the Anti-Inflammatory Effect of Acupuncture in the Ovalbumin-Induced Murine Asthma Model

2018 ◽  
Vol 36 (5) ◽  
pp. 319-326 ◽  
Author(s):  
Ming Dong ◽  
Cheng Ma ◽  
Wen-Qian Wang ◽  
Juan Chen ◽  
Ying Wei
Keyword(s):  
Lung Function ◽  
Mouse Model ◽  
Chronic Inflammation ◽  
Bronchial Asthma ◽  
Acupuncture Treatment ◽  
Dynamic Compliance ◽  
Mucus Secretion ◽  
Asthma Model ◽  
Tnf Α ◽  
Murine Asthma Model

Background Bronchial asthma is a chronic airway inflammatory disease which has three main pathological features: airway hyperresponsiveness (AHR), airway remodelling, and chronic inflammation. Acupuncture is known to be an effective integrative medical therapy that has been used in the treatment of several chronic diseases, including bronchial asthma. The aim of the current study was to evaluate the effects of acupuncture on inflammation and regulation of the IL-33/ST2 pathway in a mouse model of asthma. Methods The murine asthma model was established by both injection and inhalation of ovalbumin (OVA). Within 24 hours of the last OVA challenge, lung function was assessed by measurement of the airway resistance (RL) and lung dynamic compliance (Cdyn). Pulmonary tissues were collected for the detection of pathological changes and mucus secretion. Serum levels of tumour necrosis factor α (TNF-α), interleukin (IL)-1β, IL-33 and sST2 (secreted ST2) were detected by ELISA. Th17 cell proportions and counts in bronchoalveolar lavage fluid (BALF) were analysed by flow cytometry. Results The results showed that AHR, chronic inflammation and mucus secretion were significantly suppressed by acupuncture treatment. RL decreased while Cdyn increased after acupuncture treatment. There was an apparent decrease in the serum concentrations of certain pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-33, and an increase in sST2 level compared with untreated asthmatic mice. Acupuncture also reduced the CD4 +IL-17A+ cell proportion and counts in BALF. Conclusion Acupuncture effectively protects lung function and attenuates airway inflammation in the OVA-induced mouse model of asthma, which supports the role of acupuncture as a potential therapy in asthma treatment.

scholarly journals Single-cell transcriptional analyses of spasmolytic polypeptide-expressing metaplasia arising from acute drug injury and chronic inflammation in the stomach

Gut ◽  
2019 ◽  
Vol 69 (6) ◽  
pp. 1027-1038 ◽  
Author(s):  
Kevin A Bockerstett ◽  
Scott A Lewis ◽  
Kyle J Wolf ◽  
Christine N Noto ◽  
Nicholas M Jackson ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Single Cell ◽  
Chronic Inflammation ◽  
Intrinsic Factor ◽  
Drug Induced ◽  
Cell Hyperplasia ◽  
Tissue Samples ◽  
Spasmolytic Polypeptide ◽  
The Individual

ObjectiveSpasmolytic polypeptide-expressing metaplasia (SPEM) is a regenerative lesion in the gastric mucosa and is a potential precursor to intestinal metaplasia/gastric adenocarcinoma in a chronic inflammatory setting. The goal of these studies was to define the transcriptional changes associated with SPEM at the individual cell level in response to acute drug injury and chronic inflammatory damage in the gastric mucosa.DesignEpithelial cells were isolated from the gastric corpus of healthy stomachs and stomachs with drug-induced and inflammation-induced SPEM lesions. Single cell RNA sequencing (scRNA-seq) was performed on tissue samples from each of these settings. The transcriptomes of individual epithelial cells from healthy, acutely damaged and chronically inflamed stomachs were analysed and compared.ResultsscRNA-seq revealed a population Mucin 6 (Muc6)+gastric intrinsic factor (Gif)+ cells in healthy tissue, but these cells did not express transcripts associated with SPEM. Furthermore, analyses of SPEM cells from drug injured and chronically inflamed corpus yielded two major findings: (1) SPEM and neck cell hyperplasia/hypertrophy are nearly identical in the expression of SPEM-associated transcripts and (2) SPEM programmes induced by drug-mediated parietal cell ablation and chronic inflammation are nearly identical, although the induction of transcripts involved in immunomodulation was unique to SPEM cells in the chronic inflammatory setting.ConclusionsThese data necessitate an expansion of the definition of SPEM to include Tff2+Muc6+ cells that do not express mature chief cell transcripts such as Gif. Our data demonstrate that SPEM arises by a highly conserved cellular programme independent of aetiology and develops immunoregulatory capabilities in a setting of chronic inflammation.

Inhibition of soluble epoxide hydrolase attenuates airway remodeling in a chronic asthma model

2020 ◽  
Vol 868 ◽  
pp. 172874 ◽  
Author(s):  
Jun-xia Jiang ◽  
Yan Guan ◽  
Hui-juan Shen ◽  
Yong-liang Jia ◽  
Jian Shen ◽  
...  
Keyword(s):  
Epoxide Hydrolase ◽  
Airway Remodeling ◽  
Soluble Epoxide Hydrolase ◽  
Chronic Asthma ◽  
Asthma Model
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