scholarly journals ncRNA-regulated immune response and its role in inflammatory lung diseases

2015 ◽  
Vol 309 (10) ◽  
pp. L1076-L1087 ◽  
Author(s):  
Na Xie ◽  
Gang Liu
Keyword(s):  
Immune Response ◽  
Lung Diseases ◽  
Distress Syndrome ◽  
Noncoding Rnas ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Innate And Adaptive Immunity ◽  
Abnormal Immune Response ◽  
Protein Molecules

Despite the greatly expanded knowledge on the regulation of immune response by protein molecules, there is increasing understanding that noncoding RNAs (ncRNAs) are also an integral component of this regulatory network. Abnormal immune response serves a central role in the initiation, progression, and exacerbation of inflammatory lung diseases, such as asthma, chronic obstructive pulmonary disease, cystic fibrosis, and acute respiratory distress syndrome/acute lung injury. Dysregulation of ncRNAs has been linked to various immunopathologies. In this review, we highlighted the role of ncRNAs in the regulation of innate and adaptive immunity and summarized recent findings that ncRNAs participate in the pathogenesis of inflammatory lung diseases via their regulation of pulmonary immunity. We also discussed therapeutic potentials for targeting ncRNAs to treat these lung disorders.

scholarly journals The Role of Connexin 43 in Lung Disease

Life ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 363
Author(s):  
Julie A. Swartzendruber ◽  
Bruce J. Nicholson ◽  
Ashlesh K. Murthy
Keyword(s):  
Lung Disease ◽  
Lung Diseases ◽  
Connexin 43 ◽  
Distress Syndrome ◽  
Cell Types ◽  
Mortality Rates ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Junction Proteins

The term lung disease describes a broad category of disorders that impair lung function. More than 35 million Americans have a preventable chronic lung disease with high mortality rates due to limited treatment efficacy. The recent increase in patients with lung disease highlights the need to increase our understanding of mechanisms driving lung inflammation. Connexins, gap junction proteins, and more specifically connexin 43 (Cx43), are abundantly expressed in the lung and are known to play a role in lung diseases. This review focuses on the role of Cx43 in pathology associated with acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD) and asthma. Additionally, we discuss the role of Cx43 in preventing disease through the transfer of mitochondria between cells. We aim to highlight the need to better understand what cell types are expressing Cx43 and how this expression influences lung disease.

scholarly journals Cell therapy for lung disease

2017 ◽  
Vol 26 (144) ◽  
pp. 170044 ◽  
Author(s):  
Sabine Geiger ◽  
Daniela Hirsch ◽  
Felix G. Hermann
Keyword(s):  
Clinical Studies ◽  
Therapeutic Approach ◽  
Lung Diseases ◽  
Distress Syndrome ◽  
Treatment Options ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Cell Therapies ◽  
Promising Therapeutic Approach ◽  
Preclinical And Clinical Studies

Besides cancer and cardiovascular diseases, lung disorders are a leading cause of morbidity and death worldwide. For many disease conditions no effective and curative treatment options are available. Cell therapies offer a novel therapeutic approach due to their inherent anti-inflammatory and anti-fibrotic properties. Mesenchymal stem/stromal cells (MSC) are the most studied cell product. Numerous preclinical studies demonstrate an improvement of disease-associated parameters after MSC administration in several lung disorders, including chronic obstructive pulmonary disease, acute respiratory distress syndrome and idiopathic pulmonary fibrosis. Furthermore, results from clinical studies using MSCs for the treatment of various lung diseases indicate that MSC treatment in these patients is safe. In this review we summarise the results of preclinical and clinical studies that indicate that MSCs are a promising therapeutic approach for the treatment of lung diseases. Nevertheless, further investigations are required.

Bedside evaluation of the resistance of large and medium pulmonary veins in various lung diseases

1992 ◽  
Vol 72 (3) ◽  
pp. 998-1003 ◽  
Author(s):  
J. L. Teboul ◽  
P. Andrivet ◽  
M. Ansquer ◽  
M. Besbes ◽  
N. Rekik ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Lung Diseases ◽  
Distress Syndrome ◽  
Pulmonary Veins ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Wedge Pressure ◽  
Normal Lungs

To evaluate the contribution of large and medium pulmonary veins to the total pulmonary vascular resistance in various human lung diseases, we compared in 64 patients the pulmonary arterial proximal wedge pressure (Ppw), obtained when the balloon of a 7F pulmonary artery catheter was inflated with 1.5 ml air, with the distal wedge pressure (Pdw), obtained after the tip of the catheter was advanced until wedged in a small artery without balloon inflation. Ppw, reflecting the pressure in a large pulmonary vein, approximates the left atrial pressure, whereas Pdw reflects the pressure in a smaller pulmonary vein. Pdw was greater than Ppw in all 64 patients. The Pdw-Ppw gradient was 1.1 +/- 0.5 mmHg in nine patients with normal lungs and was significantly higher in 13 patients with chronic congestive heart failure (3.8 +/- 0.8 mmHg, P less than 0.01) and in 22 patients with adult respiratory distress syndrome (3.8 +/- 0.8 mmHg; P less than 0.01), but not in 20 patients with chronic obstructive pulmonary disease (1.8 +/- 0.7 mmHg). The distribution of the pulmonary vascular resistance was clearly different among the four groups. The fraction of the total pulmonary vascular resistance attributable to large and medium pulmonary veins was significantly increased (P less than 0.01) in adult respiratory distress syndrome (27.5 +/- 12%) and cardiac patients (27.5 +/- 9%) compared with patients with chronic obstructive pulmonary disease (13 +/- 5%) and normal lungs (13.5 +/- 6%).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Smoking and interstitial lung diseases

2015 ◽  
Vol 24 (137) ◽  
pp. 428-435 ◽  
Author(s):  
George A. Margaritopoulos ◽  
Eirini Vasarmidi ◽  
Joseph Jacob ◽  
Athol U. Wells ◽  
Katerina M. Antoniou
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Langerhans Cell Histiocytosis ◽  
Lung Diseases ◽  
Interstitial Lung Diseases ◽  
Lung Damage ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Pulmonary Langerhans Cell Histiocytosis

For many years has been well known that smoking could cause lung damage. Chronic obstructive pulmonary disease and lung cancer have been the two most common smoking-related lung diseases. In the recent years, attention has also focused on the role of smoking in the development of interstitial lung diseases (ILDs). Indeed, there are three diseases, namely respiratory bronchiolitis-associated ILD, desquamative interstitial pneumonia and pulmonary Langerhans cell histiocytosis, that are currently considered aetiologically linked to smoking and a few others which are more likely to develop in smokers. Here, we aim to focus on the most recent findings regarding the role of smoking in the pathogenesis and clinical behaviour of ILDs.

scholarly journals Interleukin-36 Cytokines in Infectious and Non-Infectious Lung Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Hernán F. Peñaloza ◽  
Rick van der Geest ◽  
Joel A. Ybe ◽  
Theodore J. Standiford ◽  
Janet S. Lee
Keyword(s):  
Infectious Diseases ◽  
Lung Diseases ◽  
Skin Diseases ◽  
Inflammatory Diseases ◽  
Lymphoid Cells ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Inflammatory Conditions ◽  
Inflammatory Processes

The IL-36 family of cytokines were identified in the early 2000’s as a new subfamily of the IL-1 cytokine family, and since then, the role of IL-36 cytokines during various inflammatory processes has been characterized. While most of the research has focused on the role of these cytokines in autoimmune skin diseases such as psoriasis and dermatitis, recent studies have also shown the importance of IL-36 cytokines in the lung inflammatory response during infectious and non-infectious diseases. In this review, we discuss the biology of IL-36 cytokines in terms of how they are produced and activated, as well as their effects on myeloid and lymphoid cells during inflammation. We also discuss the role of these cytokines during lung infectious diseases caused by bacteria and influenza virus, as well as other inflammatory conditions in the lungs such as allergic asthma, lung fibrosis, chronic obstructive pulmonary disease, cystic fibrosis and cancer. Finally, we discuss the current therapeutic advances that target the IL-36 pathway and the possibility to extend these tools to treat lung inflammatory diseases.

scholarly journals The role of the microbiota components in modification of the immune response in some cases of chronic obstructive pulmonary disease

2017 ◽  
Vol 16 (2) ◽  
pp. 125-135
Author(s):  
Natalia A. Kirillova ◽  
Ksenia V. Nevskaya ◽  
Vyacheslav A. Petrov ◽  
Julia B. Dorofeeva ◽  
Sergey V. Fedosenko ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Immune Response ◽  
Pulmonary Disease ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

scholarly journals Role of Non-Coding RNAs in Post-Transcriptional Regulation of Lung Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Dharmendra Kumar Soni ◽  
Roopa Biswas
Keyword(s):  
Transcriptional Regulation ◽  
Lung Diseases ◽  
Fine Tuning ◽  
Chronic Obstructive ◽  
Biological Processes ◽  
Obstructive Pulmonary Disease ◽  
Non Coding Rnas ◽  
Specific Tissue ◽  
Post Transcriptional Regulation

Non-coding RNAs (ncRNAs), notably microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), have recently gained increasing consideration because of their versatile role as key regulators of gene expression. They adopt diverse mechanisms to regulate transcription and translation, and thereby, the function of the protein, which is associated with several major biological processes. For example, proliferation, differentiation, apoptosis, and metabolic pathways demand fine-tuning for the precise development of a specific tissue or organ. The deregulation of ncRNA expression is concomitant with multiple diseases, including lung diseases. This review highlights recent advances in the post-transcriptional regulation of miRNAs and lncRNAs in lung diseases such as asthma, chronic obstructive pulmonary disease, cystic fibrosis, and idiopathic pulmonary fibrosis. Further, we also discuss the emerging role of ncRNAs as biomarkers as well as therapeutic targets for lung diseases. However, more investigations are required to explore miRNAs and lncRNAs interaction, and their function in the regulation of mRNA expression. Understanding these mechanisms might lead to early diagnosis and the development of novel therapeutics for lung diseases.

scholarly journals Use of nonhuman primates in obstructive lung disease research – is it required?

2017 ◽  
Vol 4 (1) ◽  
pp. 131-142
Author(s):  
Franziska Dahlmann ◽  
Katherina Sewald
Keyword(s):  
Obstructive Lung Disease ◽  
Lung Diseases ◽  
Nonhuman Primates ◽  
Animal Experiments ◽  
Alternative Methods ◽  
Chronic Obstructive ◽  
Therapeutic Approaches ◽  
Obstructive Pulmonary Disease ◽  
Disease Research

Abstract. In times of increasing costs for health insurances, obstructive lung diseases are a burden for both the patients and the economy. Pulmonary symptoms of asthma and chronic obstructive pulmonary disease (COPD) are similar; nevertheless, the diseases differ in pathophysiology and therapeutic approaches. Novel therapeutics are continuously developed, and nonhuman primates (NHPs) provide valuable models for investigating novel biologicals regarding efficacy and safety.This review discusses the role of nonhuman primate models for drug development in asthma and COPD and investigates whether alternative methods are able to prevent animal experiments.

scholarly journals Dysregulation of the glutaredoxin/S-glutathionylation redox axis in lung diseases

2020 ◽  
Vol 318 (2) ◽  
pp. C304-C327 ◽  
Author(s):  
Shi B. Chia ◽  
Evan A. Elko ◽  
Reem Aboushousha ◽  
Allison M. Manuel ◽  
Cheryl van de Wetering ◽  
...  
Keyword(s):  
Lung Diseases ◽  
Defense Mechanism ◽  
Protein S ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Mixed Disulfide ◽  
Glutathione S Transferases ◽  
And Function ◽  
Redox Buffer

Glutathione is a major redox buffer, reaching millimolar concentrations within cells and high micromolar concentrations in airways. While glutathione has been traditionally known as an antioxidant defense mechanism that protects the lung tissue from oxidative stress, glutathione more recently has become recognized for its ability to become covalently conjugated to reactive cysteines within proteins, a modification known as S-glutathionylation (or S-glutathiolation or protein mixed disulfide). S-glutathionylation has the potential to change the structure and function of the target protein, owing to its size (the addition of three amino acids) and charge (glutamic acid). S-glutathionylation also protects proteins from irreversible oxidation, allowing them to be enzymatically regenerated. Numerous enzymes have been identified to catalyze the glutathionylation/deglutathionylation reactions, including glutathione S-transferases and glutaredoxins. Although protein S-glutathionylation has been implicated in numerous biological processes, S-glutathionylated proteomes have largely remained unknown. In this paper, we focus on the pathways that regulate GSH homeostasis, S-glutathionylated proteins, and glutaredoxins, and we review methods required toward identification of glutathionylated proteomes. Finally, we present the latest findings on the role of glutathionylation/glutaredoxins in various lung diseases: idiopathic pulmonary fibrosis, asthma, and chronic obstructive pulmonary disease.

scholarly journals The Role of Macrophages in the Development of Acute and Chronic Inflammatory Lung Diseases

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 897
Author(s):  
Jae-Won Lee ◽  
Wanjoo Chun ◽  
Hee Jae Lee ◽  
Jae-Hong Min ◽  
Seong-Man Kim ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Lung Diseases ◽  
Inflammatory Responses ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Adaptive Immune ◽  
Activation Of Transcription ◽  
Organ Systems ◽  
Underlying Mechanisms

Macrophages play an important role in the innate and adaptive immune responses of organ systems, including the lungs, to particles and pathogens. Cumulative results show that macrophages contribute to the development and progression of acute or chronic inflammatory responses through the secretion of inflammatory cytokines/chemokines and the activation of transcription factors in the pathogenesis of inflammatory lung diseases, such as acute lung injury (ALI), acute respiratory distress syndrome (ARDS), ARDS related to COVID-19 (coronavirus disease 2019, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)), allergic asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). This review summarizes the functions of macrophages and their associated underlying mechanisms in the development of ALI, ARDS, COVID-19-related ARDS, allergic asthma, COPD, and IPF and briefly introduces the acute and chronic experimental animal models. Thus, this review suggests an effective therapeutic approach that focuses on the regulation of macrophage function in the context of inflammatory lung diseases.

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