scholarly journals Role of specialized pro-resolving lipid mediators in pulmonary inflammation diseases: mechanisms and development

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Ailin Yang ◽  
Yanjun Wu ◽  
Ganggang Yu ◽  
Haoyan Wang
Keyword(s):  
Immune Cells ◽  
Immune Modulation ◽  
Respiratory Diseases ◽  
Preventive Measures ◽  
Pulmonary Inflammation ◽  
Lipid Mediators ◽  
Pulmonary Diseases ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

AbstractInflammation is an essential mechanism of various diseases. The development and resolution of inflammation are complex immune-modulation processes which induce the involvement of various types of immune cells. Specialized pro-resolving lipid mediators (SPMs) have been demonstrated to be signaling molecules in inflammation. SPMs are involved in the pathophysiology of different diseases, especially respiratory diseases, including asthma, pneumonia, and chronic obstructive pulmonary disease. All of these diseases are related to the inflammatory response and its persistence. Therefore, a deeper understanding of the mechanisms and development of inflammation in respiratory disease, and the roles of the SPM family in the resolution process, might be useful in the quest for novel therapies and preventive measures for pulmonary diseases.

scholarly journals Role of exosomes in pathogenesis of pulmonary diseases (review)

2020 ◽  
pp. 107-117
Author(s):  
S. S. Tseluyko ◽  
V. O. Derevyannaya
Keyword(s):  
Lung Cancer ◽  
Respiratory System ◽  
Intercellular Space ◽  
Respiratory Diseases ◽  
Biological Fluids ◽  
Pulmonary Diseases ◽  
Chronic Obstructive ◽  
Signaling Proteins ◽  
Obstructive Pulmonary Disease

The article presents modern data on exosomes - microscopic extracellular vesicles with a diameter of 30-180 nanometers, released into the intercellular space by cells of the respiratory organs. The cells of the body’s respiratory system secrete exosomes into the intercellular space in a normal state, as well as during the development of the disease. The concentration of exosomes depends on the type of cell and includes mRNA, miRNAs, DNA and signaling proteins. Some exosomal proteins, such as CD63, CD81, CD9, CD24 and heat shock protein (Hsp70) are universal and they are usually used as exosomal markers. In respiratory diseases, in particular in patients with chronic obstructive pulmonary disease, IL-1P and miRNAs such as miR-15b, miR-223, miR-1274a, miR-424, mir-210 are significantly increased; miR-21 is the most common miRNA isolated from lung tissue, increased expression of this RNA is associated with symptoms of asthma, idiopathic pulmonary fibrosis and lung cancer. Exosome analysis makes it possible to distinguish between pulmonary and extrapulmonary forms of tuberculosis based on exosomal markers such as MPT64. Circulating exosomes are stable in biological fluids; therefore, analysis of exosomal microRNAs may indicate the state of the human respiratory system. This review opens up the possibility of using new diagnostic and therapeutic targets for various diseases of the respiratory system.

scholarly journals Role of Farnesoid X Receptor in the Pathogenesis of Respiratory Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Jin-nan Wu ◽  
Jian-rong Chen ◽  
Jin-liang Chen
Keyword(s):  
Bile Acid ◽  
Respiratory Diseases ◽  
The Body ◽  
Farnesoid X Receptor ◽  
Bile Acid Metabolism ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Target Organs ◽  
The Stability

Farnesoid X receptor (FXR) is a bile acid receptor encoded by the Nr1h4 gene. FXR plays an important role in maintaining the stability of the internal environment and the integrity of many organs, including the liver and intestines. The expression of FXR in nondigestible tissues other than in the liver and small intestine is known as the expression of “nonclassical” bile acid target organs, such as blood vessels and lungs. In recent years, several studies have shown that FXR is widely involved in the pathogenesis of various respiratory diseases, such as chronic obstructive pulmonary disease, bronchial asthma, and idiopathic pulmonary fibrosis. Moreover, a number of works have confirmed that FXR can regulate the bile acid metabolism in the body and exert its anti-inflammatory and antifibrotic effects in the airways and lungs. In addition, FXR may be used as a potential therapeutic target for some respiratory diseases. For example, FXR can regulate the tumor microenvironment by regulating the balance of inflammatory and immune responses in the body to promote the occurrence and development of non-small-cell lung cancer (NSCLC), thereby being considered a potential target for immunotherapy of NSCLC. In this article, we provide an overview of the internal relationship between FXR and respiratory diseases to track the progress that has been achieved thus far in this direction and suggest potential therapeutic prospects of FXR in respiratory diseases.

scholarly journals High Frequency of Viral Co-Detections in Acute Bronchiolitis

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 990
Author(s):  
Hortense Petat ◽  
Vincent Gajdos ◽  
François Angoulvant ◽  
Pierre-Olivier Vidalain ◽  
Sandrine Corbet ◽  
...  
Keyword(s):  
Respiratory Diseases ◽  
Virus Detection ◽  
Public Health Issue ◽  
Chronic Obstructive ◽  
Acute Bronchiolitis ◽  
Obstructive Pulmonary Disease ◽  
Chronic Respiratory Diseases ◽  
Coronavirus Infection ◽  
Syncytial Virus

Over two years (2012–2014), 719 nasopharyngeal samples were collected from 6-week- to 12-month-old infants presenting at the emergency department with moderate to severe acute bronchiolitis. Viral testing was performed, and we found that 98% of samples were positive, including 90% for respiratory syncytial virus, 34% for human rhino virus, and 55% for viral co-detections, with a predominance of RSV/HRV co-infections (30%). Interestingly, we found that the risk of being infected by HRV is higher in the absence of RSV, suggesting interferences or exclusion mechanisms between these two viruses. Conversely, coronavirus infection had no impact on the likelihood of co-infection involving HRV and RSV. Bronchiolitis is the leading cause of hospitalizations in infants before 12 months of age, and many questions about its role in later chronic respiratory diseases (asthma and chronic obstructive pulmonary disease) exist. The role of virus detection and the burden of viral codetections need to be further explored, in order to understand the physiopathology of chronic respiratory diseases, a major public health issue.

scholarly journals Possible Role of Serum Leptin as Biomarker in COPD

Folia Medica ◽  
2019 ◽  
Vol 61 (4) ◽  
pp. 512-521
Author(s):  
Yanitsa A. Zhelyazkova ◽  
Tanya T. Tacheva ◽  
Dimo M. Dimov ◽  
Denitsa G. Vlaykova ◽  
Aneliya V. Bivolarska ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Respiratory Diseases ◽  
Smoking Habits ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Serum Leptin ◽  
Copd Patients ◽  
Severe Copd

Leptin is one of the adipokines shown to exert a significant effect in respiratory diseases, including chronic obstructive pulmonary disease (COPD).The aim of the present study was to evaluate the possible role of serum leptin as biomarker in COPD.The serum leptin levels were assessed in 58 patents with stable COPD and 21 controls applying ELISA method.The leptin levels were higher, although not significantly, in COPD patients than in controls (221.52&plusmn;24.28(SE) vs. 165.04&plusmn;26.01 pg/ml, p=0.197). This tendency turned out significant when only females were compared (414.60&plusmn;60.63 vs. 219.40&plusmn;44.15 pg/ml, p=0.038). The levels of leptin were highly dependent on the BMI both in COPD patients (p<0.001) and in controls (p=0.024): they were the highest in obese individuals and decreased with reducing the BMI.In the COPD group, women had significantly higher leptin levels than men (p<0.0001) independent of the BMI. The non-smoking patients had significantly higher leptin levels than ex-smokers (p=0.007) and current smokers (p=0.007). In patients with BMI above 25, several associations were observed: patients with mild COPD had higher serum leptin level than those with severe or very severe COPD (p=0.038); the leptin levels correlated positively with FEV1% (r= 0.304, p=0.045) and FEV1/FVC ratio (I= 0.348, p=0.021), and tended to correlate negatively with ABCD GOLD groups (Rho=-0.300, p=0.043) and with the CAT points (Rho=-0.258, p=0.091); the leptin levels below 300 ng/ml determined 4.08-fold higher risk for more severe COPD.The results of our study confirm that the serum leptin levels depend significantly on the BMI and are interfered by gender and smoking habits. However, this adipokine cannot be used as a serum biomarker for distinguishing COPD patients, but its decrease might be associated with aggravation of the disease.

scholarly journals The Role of Innate Lymphoid Cells in Chronic Respiratory Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Amy T. Hsu ◽  
Timothy A. Gottschalk ◽  
Evelyn Tsantikos ◽  
Margaret L. Hibbs
Keyword(s):  
Immune System ◽  
Respiratory Diseases ◽  
Pulmonary Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Chronic Obstructive ◽  
Chronic Respiratory Diseases ◽  
Chronic Lung Diseases ◽  
Pulmonary Immune System

The lung is a vital mucosal organ that is constantly exposed to the external environment, and as such, its defenses are continuously under threat. The pulmonary immune system has evolved to sense and respond to these danger signals while remaining silent to innocuous aeroantigens. The origin of the defense system is the respiratory epithelium, which responds rapidly to insults by the production of an array of mediators that initiate protection by directly killing microbes, activating tissue-resident immune cells and recruiting leukocytes from the blood. At the steady-state, the lung comprises a large collection of leukocytes, amongst which are specialized cells of lymphoid origin known as innate lymphoid cells (ILCs). ILCs are divided into three major helper-like subsets, ILC1, ILC2 and ILC3, which are considered the innate counterparts of type 1, 2 and 17 T helper cells, respectively, in addition to natural killer cells and lymphoid tissue inducer cells. Although ILCs represent a small fraction of the pulmonary immune system, they play an important role in early responses to pathogens and facilitate the acquisition of adaptive immunity. However, it is now also emerging that these cells are active participants in the development of chronic lung diseases. In this mini-review, we provide an update on our current understanding of the role of ILCs and their regulation in the lung. We summarise how these cells and their mediators initiate, sustain and potentially control pulmonary inflammation, and their contribution to the respiratory diseases chronic obstructive pulmonary disease (COPD) and asthma.

scholarly journals The Human Microbiome, an Emerging Key-Player in the Sex Gap in Respiratory Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Clémence Beauruelle ◽  
Charles-Antoine Guilloux ◽  
Claudie Lamoureux ◽  
Geneviève Héry-Arnaud
Keyword(s):  
Gut Microbiome ◽  
Immune Modulation ◽  
Respiratory Diseases ◽  
Pulmonary Infection ◽  
Human Microbiome ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
The Past ◽  
Lung Microbiome ◽  
Males And Females

The sex gap is well-documented in respiratory diseases such as cystic fibrosis and chronic obstructive pulmonary disease. While the differences between males and females in prevalence, severity and prognosis are well-established, the pathophysiology of the sex difference has been poorly characterized to date. Over the past 10 years, metagenomics-based studies have revealed the presence of a resident microbiome in the respiratory tract and its central role in respiratory disease. The lung microbiome is associated with host immune response and health outcomes in both animal models and patient cohorts. The study of the lung microbiome is therefore an interesting new avenue to explore in order to understand the sex gap observed in respiratory diseases. Another important parameter to consider is the gut-lung axis, since the gut microbiome plays a crucial role in distant immune modulation in respiratory diseases, and an intestinal “microgenderome” has been reported: i.e., sexual dimorphism in the gut microbiome. The microgenderome provides new pathophysiological clues, as it defines the interactions between microbiome, sex hormones, immunity and disease susceptibility. As research on the microbiome is increasing in volume and scope, the objective of this review was to describe the state-of-the-art on the sex gap in respiratory medicine (acute pulmonary infection and chronic lung disease) in the light of the microbiome, including evidence of local (lung) or distant (gut) contributions to the pathophysiology of these diseases.

scholarly journals DGKα in Neutrophil Biology and Its Implications for Respiratory Diseases

2019 ◽  
Vol 20 (22) ◽  
pp. 5673 ◽  
Author(s):  
Gianluca Baldanzi ◽  
Mario Malerba
Keyword(s):  
Respiratory Diseases ◽  
Genetic Diseases ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Rare Genetic Diseases ◽  
Antitrypsin Deficiency ◽  
Alpha 1 Antitrypsin Deficiency ◽  
Alpha 1 Antitrypsin

Diacylglycerol kinases (DGKs) play a key role in phosphoinositide signaling by removing diacylglycerol and generating phosphatidic acid. Besides the well-documented role of DGKα and DGKζ as negative regulators of lymphocyte responses, a robust body of literature points to those enzymes, and specifically DGKα, as crucial regulators of leukocyte function. Upon neutrophil stimulation, DGKα activation is necessary for migration and a productive response. The role of DGKα in neutrophils is evidenced by its aberrant behavior in juvenile periodontitis patients, which express an inactive DGKα transcript. Together with in vitro experiments, this suggests that DGKs may represent potential therapeutic targets for disorders where inflammation, and neutrophils in particular, plays a major role. In this paper we focus on obstructive respiratory diseases, including asthma and chronic obstructive pulmonary disease (COPD), but also rare genetic diseases such as alpha-1-antitrypsin deficiency. Indeed, the biological role of DGKα is understudied outside the T lymphocyte field. The recent wave of research aiming to develop novel and specific inhibitors as well as KO mice will allow a better understanding of DGK’s role in neutrophilic inflammation. Better knowledge and pharmacologic tools may also allow DGK to move from the laboratory bench to clinical trials.

scholarly journals The role of hyaluronan in the pathobiology and treatment of respiratory disease

2016 ◽  
Vol 310 (9) ◽  
pp. L785-L795 ◽  
Author(s):  
Stavros Garantziotis ◽  
Martin Brezina ◽  
Paolo Castelnuovo ◽  
Lorenzo Drago
Keyword(s):  
Respiratory Diseases ◽  
Degradation Products ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Cell Matrix ◽  
Airway Diseases ◽  
Naturally Occurring ◽  
Tissue Healing ◽  
And Migration

Hyaluronan, a ubiquitous naturally occurring glycosaminoglycan, is a major component of the extracellular matrix, where it participates in biological processes that include water homeostasis, cell-matrix signaling, tissue healing, inflammation, angiogenesis, and cell proliferation and migration. There are emerging data that hyaluronan and its degradation products have an important role in the pathobiology of the respiratory tract. We review the role of hyaluronan in respiratory diseases and present evidence from published literature and from clinical practice supporting hyaluronan as a novel treatment for respiratory diseases. Preliminary data show that aerosolized exogenous hyaluronan has beneficial activity against airway inflammation, protects against bronchial hyperreactivity and remodeling, and disrupts the biofilm associated with chronic infection. This suggests a role in airway diseases with a predominant inflammatory component such as rhinosinusitis, asthma, chronic obstructive pulmonary disease, cystic fibrosis, and primary ciliary dyskinesia. The potential for hyaluronan to complement conventional therapy will become clearer when data are available from controlled trials in larger patient populations.

scholarly journals Understanding the role of neutrophils in chronic inflammatory airway disease

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 557 ◽  
Author(s):  
Alice E Jasper ◽  
William J McIver ◽  
Elizabeth Sapey ◽  
Georgia M Walton
Keyword(s):  
Cystic Fibrosis ◽  
Immune Cell ◽  
Pulmonary Inflammation ◽  
Neutrophil Migration ◽  
Airway Disease ◽  
Chronic Obstructive ◽  
Pathological Features ◽  
Obstructive Pulmonary Disease ◽  
Species Production

Airway neutrophilia is a common feature of many chronic inflammatory lung diseases and is associated with disease progression, often regardless of the initiating cause. Neutrophils and their products are thought to be key mediators of the inflammatory changes in the airways of patients with chronic obstructive pulmonary disease (COPD) and have been shown to cause many of the pathological features associated with disease, including emphysema and mucus hypersecretion. Patients with COPD also have high rates of bacterial colonisation and recurrent infective exacerbations, suggesting that neutrophil host defence mechanisms are impaired, a concept supported by studies showing alterations to neutrophil migration, degranulation and reactive oxygen species production in cells isolated from patients with COPD. Although the role of neutrophils is best described in COPD, many of the pathological features of this disease are not unique to COPD and also feature in other chronic inflammatory airway diseases, including asthma, cystic fibrosis, alpha-1 anti-trypsin deficiency, and bronchiectasis. There is increasing evidence for immune cell dysfunction contributing to inflammation in many of these diseases, focusing interest on the neutrophil as a key driver of pulmonary inflammation and a potential therapeutic target than spans diseases. This review discusses the evidence for neutrophilic involvement in COPD and also considers their roles in alpha-1 anti-trypsin deficiency, bronchiectasis, asthma, and cystic fibrosis. We provide an in-depth assessment of the role of the neutrophil in each of these conditions, exploring recent advances in understanding, and finally discussing the possibility of common mechanisms across diseases.

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