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New Advances in Induced Airway and Lung Inflammation, and Intervention...
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New Advances in Induced Airway and Lung Inflammation, and Intervention of Therapeutic Strategies

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Pulmonology".

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 15637

Special Issue Editor

Dr. Chuen-Mao Yang

E-Mail Website
Guest Editor
Graduate Institute of Biomedical and Pharmaceutical Science, College of Medicine, Fu Jen Catholic University, New Taipei City 242062, Taiwan
Interests: signaling transduction; inflammation; antioxidants; anti-inflammation; neuroaging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Many diseases, such as acute respiratory distress syndrome, asthma, cystic fibrosis, and chronic obstructive pulmonary disease, have one thing in common: lung inflammation. Animal and human inhalation of or exposure to smoking, air pollution, viruses, and bacteria can stimulate the generation of ROS, which are associated with airway and lung inflammatory diseases.

Respiratory inflammation is complicated by the involvement of various types of cells, pro-inflammatory cytokines, and other factors. In particular, cytokines, chemokines, and endotoxins have been implicated in the pathogenesis of pulmonary inflammation. Its pathogenesis is mediated through activation of various intracellular signaling components and transcription factors that lead to the expression of inflammatory proteins such as cytokines, chemokines, and adhesion molecules. Injurious environmental stimuli can access the lung either through the airways or the pulmonary and systemic circulations. The time course and intensity of responses in resident and circulating cells may be regulated by various inflammatory signaling that modulate both key inflammatory signaling transduction pathways and target proteins involved in airway and lung inflammation.

Yet, the complexity of the inflammation mechanism and combating inflammation have continued to create challenges. The interplay between oxidative stress and expression of inflammatory proteins induced by pro-inflammatory mediators leading to airway and lung inflammation needs to be further discussed. Knowledge of the mechanisms of oxidative stress regulation could lead to the pharmacological manipulation of antioxidants and anti-inflammation in airway and lung inflammation.

Thus, this Special Issue focuses on new advances on induced airway and lung inflammation, and intervention of therapeutic strategies. Research articles, new ideas, and development of potential interventions that manage and protect against airway and lung inflammation are welcome to enlighten, inspire, and provide a more comprehensive picture and understanding of this area of expertise.

Dr. Chuen-Mao Yang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (3 papers)

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Research

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12 pages, 4091 KiB  
Article
Liver X Receptor Expression and Pentraxin 3 Production in Chronic Rhinosinusitis and Sinonasal Mucosal Fibroblast Cells
by Yih-Jeng Tsai, Ping-Hung Shen, Sheng-Dean Luo and Wen-Bin Wu
J. Clin. Med. 2021, 10(3), 452; https://doi.org/10.3390/jcm10030452 - 25 Jan 2021
Cited by 1 | Viewed by 1962
Abstract
The long pentraxin 3 (PTX3) is a prototypic molecule for recognizing pathogens. Liver X receptors (LXRs), belonging to nuclear receptors (NRs) for cholesterol metabolism through heterodimerizing with other NRs, were recently reported to participate in inflammation. However, their roles in chronic rhinosinusitis without [...] Read more.
The long pentraxin 3 (PTX3) is a prototypic molecule for recognizing pathogens. Liver X receptors (LXRs), belonging to nuclear receptors (NRs) for cholesterol metabolism through heterodimerizing with other NRs, were recently reported to participate in inflammation. However, their roles in chronic rhinosinusitis without nasal polyps (CRSsNP) are unclear. Therefore, this study was sought to explore roles of LXRs in chronic rhinosinusitis (CRS) sinonasal tissues and derived fibroblasts. Immunohistochemistry indicated that LXRα and β expression and lipid/fat deposition were differentially expressed in the control and CRSsNP nasal mucosa. GW7647 (a peroxisome proliferator activated receptor α (PPARα) agonist) and GW3965 (a dual agonist for LXRα and β) significantly caused PTX3 induction in the fibroblast cells. GW3965 induced PTX3 mRNA and protein expression, and the induction substantially led to PTX3 secretion. Meanwhile, an endogenous agonist-cholesterol had a similar enhancing effect on the induction of PTX3 protein. LXR siRNA knockdown to lower LXRα or β expression significantly compromised PTX3 induction. Interestingly, GW3965 also induced phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) activation and its inhibition reduced PTX3 expression. Collectively, we demonstrated here for the first time that CRSsNP nasal mucosa differentially expresses LXRα and β and deposits lipids/fats that may contain cholesterol metabolites to activate LXRs. Activation of LXRs leads to PTX3 production in sinonasal mucosa-derived fibroblasts. Our previous study showed PTX3 overexpression in the nasal cavity of CRSsNP, whereas this study highlights that cholesterol metabolites and LXR activation regulate PTX3 production and may contribute to antimicrobial activity and tissue repair during CRSsNP progression. Full article
(This article belongs to the Special Issue New Advances in Induced Airway and Lung Inflammation, and Intervention of Therapeutic Strategies)
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11 pages, 562 KiB  
Article
The Effect of a Pulmonary Rehabilitation on Lung Function and Exercise Capacity in Patients with Burn: A Prospective Randomized Single-Blind Study
by Yu Hui Won, Yoon Soo Cho, So Young Joo and Cheong Hoon Seo
J. Clin. Med. 2020, 9(7), 2250; https://doi.org/10.3390/jcm9072250 - 15 Jul 2020
Cited by 8 | Viewed by 3531
Abstract
We performed pulmonary function (PF) tests and factors affecting PF evaluation in 120 patients with inhalation injury to evaluate the effects of pulmonary rehabilitation (PR) in burn patients with inhalation injury. Patients were randomized into pulmonary rehabilitation (PR) group and conventional rehabilitation (CON) [...] Read more.
We performed pulmonary function (PF) tests and factors affecting PF evaluation in 120 patients with inhalation injury to evaluate the effects of pulmonary rehabilitation (PR) in burn patients with inhalation injury. Patients were randomized into pulmonary rehabilitation (PR) group and conventional rehabilitation (CON) group. PF tests, including forced vital capacity (FVC), 1-s forced expiratory volume FEV1), maximum voluntary ventilation (MVV), and respiratory muscles strength (maximal expiratory pressure (MEP) and maximal inspiratory pressure (MIP)), were measured by mouth pressure meter in the sitting position. Diffusing capacity for carbon monoxide (DLco) was determined by the single-breath carbon monoxide technique. Peak cough flow (PCF) was measured by a peak flow meter. Diaphragmatic mobility (DM) was evaluated on anteroposterior fluoroscopy. All evaluations were performed in all groups at baseline and after 12 weeks. There were no differences in evaluations between the PR group and CON group before the intervention. There were significant improvements in the PCF and MIP (%) changes, taken before and after rehabilitation in the PR group, compared with the changes in the CON group (p = 0.01, and p = 0.04). There were no significant changes in the other parameters in the PR group compared with the changes in the CON group (p > 0.05). There were significant differences in DLco (%), MIP, MIP (%), and DM between the PR group and the CON group (p = 0.02, p = 0.005, and p = 0.001) after 12 weeks of rehabilitation. There were no differences between the PR group and CON group after 12 weeks rehabilitation in the other parameters (p > 0.05). PR for patients with major burns and smoke inhalation induced improved PCF, MIP, MIP (%), DLco (%), and DM. These results show that PR should be a fundamental component of the treatment program for patients with burns. Full article
(This article belongs to the Special Issue New Advances in Induced Airway and Lung Inflammation, and Intervention of Therapeutic Strategies)
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Review

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41 pages, 3488 KiB  
Review
Volatile Organic Compounds in Exhaled Breath as Fingerprints of Lung Cancer, Asthma and COPD
by Ileana Andreea Ratiu, Tomasz Ligor, Victor Bocos-Bintintan, Chris A Mayhew and Bogusław Buszewski
J. Clin. Med. 2021, 10(1), 32; https://doi.org/10.3390/jcm10010032 - 24 Dec 2020
Cited by 91 | Viewed by 9678
Abstract
Lung cancer, chronic obstructive pulmonary disease (COPD) and asthma are inflammatory diseases that have risen worldwide, posing a major public health issue, encompassing not only physical and psychological morbidity and mortality, but also incurring significant societal costs. The leading cause of death worldwide [...] Read more.
Lung cancer, chronic obstructive pulmonary disease (COPD) and asthma are inflammatory diseases that have risen worldwide, posing a major public health issue, encompassing not only physical and psychological morbidity and mortality, but also incurring significant societal costs. The leading cause of death worldwide by cancer is that of the lung, which, in large part, is a result of the disease often not being detected until a late stage. Although COPD and asthma are conditions with considerably lower mortality, they are extremely distressful to people and involve high healthcare overheads. Moreover, for these diseases, diagnostic methods are not only costly but are also invasive, thereby adding to people’s stress. It has been appreciated for many decades that the analysis of trace volatile organic compounds (VOCs) in exhaled breath could potentially provide cheaper, rapid, and non-invasive screening procedures to diagnose and monitor the above diseases of the lung. However, after decades of research associated with breath biomarker discovery, no breath VOC tests are clinically available. Reasons for this include the little consensus as to which breath volatiles (or pattern of volatiles) can be used to discriminate people with lung diseases, and our limited understanding of the biological origin of the identified VOCs. Lung disease diagnosis using breath VOCs is challenging. Nevertheless, the numerous studies of breath volatiles and lung disease provide guidance as to what volatiles need further investigation for use in differential diagnosis, highlight the urgent need for non-invasive clinical breath tests, illustrate the way forward for future studies, and provide significant guidance to achieve the goal of developing non-invasive diagnostic tests for lung disease. This review provides an overview of these issues from evaluating key studies that have been undertaken in the years 2010–2019, in order to present objective and comprehensive updated information that presents the progress that has been made in this field. The potential of this approach is highlighted, while strengths, weaknesses, opportunities, and threats are discussed. This review will be of interest to chemists, biologists, medical doctors and researchers involved in the development of analytical instruments for breath diagnosis. Full article
(This article belongs to the Special Issue New Advances in Induced Airway and Lung Inflammation, and Intervention of Therapeutic Strategies)
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