scholarly journals MTMR14 Alleviates Chronic Obstructive Pulmonary Disease as a Regulator in Inflammation and Emphysema

2022 ◽  
Vol 2022 ◽  
pp. 1-21
Author(s):  
Yiya Gu ◽  
Jinkun Chen ◽  
Qian Huang ◽  
Yuan Zhan ◽  
Ting Wang ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Mitochondrial Function ◽  
Lavage Fluid ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients

Extensive inflammation and apoptosis in structural cells of the lung are responsible for the progression and pathogenesis of chronic obstructive pulmonary disease (COPD). Myotubularin-related protein 14 (MTMR14) has been shown to participate in various biological processes, including apoptosis, inflammation, and autophagy. Nonetheless, the role of MTMR14 in COPD remains elusive. In the present study, we explored the expression of MTMR14 in human lung tissues and investigated the effects of overexpressed MTMR14 on in vitro and in vivo COPD models. Moreover, one of the possible mechanisms of MTMR14 alleviating COPD was explored based on mitochondrial function and mitophagy homeostasis. The results showed that MTMR14 expression was reduced in COPD patients’ lungs in comparison to control subjects. MTMR14 overexpression inhibited cigarette smoke extract-induced inflammation and apoptosis and improved mitochondrial function and mitophagy in vitro. Further verification was carried out in COPD model mice. MTMR14 overexpression inhibited lung inflammation and reduced levels of IL-6 and KC in bronchoalveolar lavage fluid, as well as prevented emphysema and a decline in lung function. Furthermore, MTMR14 overexpression improved mitochondrial function and mitophagy to a certain extent. Collectively, our data support the hypothesis that MTMR14 participates in the pathogenesis of COPD. Improving mitochondrial function and mitophagy homeostasis may be one of the mechanisms by which MTMR14 alleviates COPD and may potentially be a novel therapeutic target for COPD.

scholarly journals The Role of Non-Typeable Haemophilus influenzae Biofilms in Chronic Obstructive Pulmonary Disease

2021 ◽  
Vol 11 ◽  
Author(s):  
Jake R. Weeks ◽  
Karl J. Staples ◽  
C. Mirella Spalluto ◽  
Alastair Watson ◽  
Tom M. A. Wilkinson
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Haemophilus Influenzae ◽  
Pulmonary Disease ◽  
Interspecific Interactions ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Acute Exacerbations

Non-typeable Haemophilus influenzae (NTHi) is an ubiquitous commensal-turned-pathogen that colonises the respiratory mucosa in airways diseases including Chronic Obstructive Pulmonary Disease (COPD). COPD is a progressive inflammatory syndrome of the lungs, encompassing chronic bronchitis that is characterised by mucus hypersecretion and impaired mucociliary clearance and creates a static, protective, humid, and nutrient-rich environment, with dysregulated mucosal immunity; a favourable environment for NTHi colonisation. Several recent large COPD cohort studies have reported NTHi as a significant and recurrent aetiological pathogen in acute exacerbations of COPD. NTHi proliferation has been associated with increased hospitalisation, disease severity, morbidity and significant lung microbiome shifts. However, some cohorts with patients at different severities of COPD do not report that NTHi is a significant aetiological pathogen in their COPD patients, indicating other obligate pathogens including Moraxella catarrhalis, Streptococcus pneumoniae and Pseudomonas aeruginosa as the cause. NTHi is an ubiquitous organism across healthy non-smokers, healthy smokers and COPD patients from childhood to adulthood, but it currently remains unclear why NTHi becomes pathogenic in only some cohorts of COPD patients, and what behaviours, interactions and adaptations are driving this susceptibility. There is emerging evidence that biofilm-phase NTHi may play a significant role in COPD. NTHi displays many hallmarks of the biofilm lifestyle and expresses key biofilm formation-promoting genes. These include the autoinducer-mediated quorum sensing system, epithelial- and mucus-binding adhesins and expression of a protective, self-produced polymeric substance matrix. These NTHi biofilms exhibit extreme tolerance to antimicrobial treatments and the immune system as well as expressing synergistic interspecific interactions with other lung pathogens including S. pneumoniae and M. catarrhalis. Whilst the majority of our understanding surrounding NTHi as a biofilm arises from otitis media or in-vitro bacterial monoculture models, the role of NTHi biofilms in the COPD lung is now being studied. This review explores the evidence for the existence of NTHi biofilms and their impact in the COPD lung. Understanding the nature of chronic and recurrent NTHi infections in acute exacerbations of COPD could have important implications for clinical treatment and identification of novel bactericidal targets.

scholarly journals Nutrition in chronic obstructive pulmonary disease: A review

2015 ◽  
Vol 3 (4) ◽  
pp. 151-154 ◽  
Author(s):  
Gautam Rawal ◽  
Sankalp Yadav
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Exercise Tolerance ◽  
Muscle Wasting ◽  
Nutritional Supplement ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Supplement Therapy

AbstractCachexia and muscle wasting is a frequent but partly reversible complication in patients with chronic obstructive pulmonary disease (COPD), and affects the disease progression and prognosis. Weight loss in COPD is a consequence of increased energy requirements unbalanced by dietary intake. Nutritional supplement therapy has been shown to be effective for maintaining and improving the muscle strength and exercise tolerance in poorly nourished COPD patients, thereby decreasing morbidity and mortality. This mini review discusses the role of nutritional supplement therapy in the treatment of COPD.

scholarly journals Reassessing the Role of Eosinophils as a Biomarker in Chronic Obstructive Pulmonary Disease

2019 ◽  
Vol 8 (7) ◽  
pp. 962 ◽  
Author(s):  
Tinè ◽  
Biondini ◽  
Semenzato ◽  
Bazzan ◽  
Cosio ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Inhaled Corticosteroids ◽  
Real Life ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Exacerbation Risk ◽  
Blood Eosinophils

Blood eosinophils measurement, as proxy for tissue eosinophils, has become an important biomarker for exacerbation risk and response to inhaled corticosteroids (ICS) in Chronic Obstructive Pulmonary Disease (COPD). Its use to determine the pharmacological approach is recommended in the latest COPD guidelines. The potential role of blood eosinophils is mainly based on data derived from post-hoc and retrospective analyses that showed an association between increased blood eosinophils and risk of exacerbations, as well as mitigation of this risk with ICS. Yet other publications, including studies in real life COPD, do not confirm these assumptions. Moreover, anti-eosinophil therapy targeting interleukin (IL)-5 failed to reduce exacerbations in COPD patients with high blood eosinophils, which casts significant doubts on the role of eosinophils in COPD. Furthermore, a reduction of eosinophils might be harmful since COPD patients with relatively high eosinophils have better pulmonary function, better life quality, less infections and longer survival. These effects are probably linked to the role of eosinophils in the immune response against pathogens. In conclusion, in COPD, high blood eosinophils are widely used as a biomarker for exacerbation risk and response to ICS. However, much is yet to be learned about the reasons for the high eosinophil counts, their variations and their controversial effects on the fate of COPD patients.

Erythropoietin response after correction of severe hypoxaemia due to acute respiratory failure in chronic obstructive pulmonary disease patients

2004 ◽  
Vol 106 (1) ◽  
pp. 43-51 ◽  
Author(s):  
Gordana PAVLISA ◽  
Veljko VRBANIC ◽  
Vesna KUSEC ◽  
Branimir JAKSIC
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Early Stage ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Complex Process ◽  
Severe Hypoxaemia ◽  
Physiological Research

In order to determine the initial values and dynamic changes of EPO (erythropoietin) after therapy, 57 consecutively presenting, typical COPD (chronic obstructive pulmonary disease) patients with chronic hypoxia and acute exacerbated serum EPO levels were serially measured. Initial mean EPO levels were slightly above the normal range (41.4±83.5 units/l), but in the majority of patients the initial EPO levels were significantly reduced. Following the correction of hypoxaemia, mean EPO levels decreased to 14.1±16.9 units/l (P=0.0093). However, not all COPD patients showed this pattern; in an important subset of patients (36.8%), who had initially lower EPO levels and lower erythrocyte count, EPO levels were significantly increased (by more than 60%; P=0.0028) on the second day of treatment, despite correction of the hypoxaemia. This finding was unexpected and paradoxical when compared with physiological studies addressing the same issue. The data presented support previous reports of variable EPO levels in severely hypoxic COPD patients and suggest that the haematological response is already hampered at an early stage, at the level of EPO production, and much less likely at later steps in the haemopoietic response by failure to respond to elevated EPO levels. Our data are consistent with recent discoveries that the O2 sensing and regulation of EPO production is a complex process in which multiple factors, including cytokines and therapeutic agents, play a role by enhancing or inhibiting the response. We believe that further studies on this clinical condition are complementary to basic physiological research and may help to elucidate the role of cytokines and other individual factors in complex clinical hypoxic situations.

scholarly journals Chronic Obstructive Pulmonary Disease (COPD) and Its Association with Lung Cancer: Molecular Mechanism and Therapeutic Targets

2021 ◽  
Vol 8 (2) ◽  
Author(s):  
Shanmugam G ◽  
◽  
Rakshit S ◽  
Sarkar K ◽  
◽  
...  
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Therapeutic Targets ◽  
Epidemiological Studies ◽  
Chronic Obstructive ◽  
Lung Carcinogenesis ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients

Chronic Obstructive Pulmonary Disease (COPD) and Lung cancer are the major reasons for lung disease-related mortality worldwide. Chronic inflammation is a key attribute of COPD and a potential driver of lung carcinogenesis. Among various environmental risk factors, cigarette smoke plays a crucial role in the development and progression of COPD and lung cancer. Several epidemiological studies show that COPD patients are at a greater risk of developing lung cancer independently of cigarette smoking which suggests the role of genetic predisposition in the disease development. Uncovering the mechanistic link between these two diseases is hampered due to their heterogeneous nature: each is characterized by several sub-phenotypes of diseases. This review focuses on the nature of the link between the two diseases and specific mechanisms that occur in both COPD and lung cancer, some of the therapeutic targets which are currently employed, and the role of gene-editing technology to combat these debilitating lung-inflammatory disorders.

scholarly journals Diaphragm Ultrasound Distinguishes Exacerbation From Stable Status in Chronic Obstructive Pulmonary Disease

2021 ◽  
Author(s):  
Tai Joon An ◽  
Yeun Jie Yoo ◽  
Jeong Uk Lim ◽  
Wan Seo ◽  
Chan Kwon Park ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Operating Characteristic ◽  
Forced Expiratory Volume ◽  
Diaphragm Muscle ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
The Status

Abstract Background: The importance of evaluating the diaphragm muscle in chronic obstructive pulmonary disease (COPD) is widely accepted. However, the role of diaphragm ultrasound (DUS) in COPD is not fully understood. We set this study to evaluate the role of DUS for distinguishing the status of COPD. Methods: COPD patients who underwent DUS were enrolled between March 2020 and November 2020. The diaphragm thickening fraction (TFmax) and diaphragm excursion (DEmax) during maximal deep breathing were measured. Patients were divided into exacerbation and stable groups. Demographics, lung function, and DUS findings were compared between the two groups. Receiver operating characteristic (ROC) curve and univariate/multivariate logistic regression analyses were performed.Results: Fifty-five patients were enrolled. The exacerbation group had a lower body mass index (BMI) (20.9 vs. 24.2, p = 0.003), lower TFmax (94.8 ± 8.2% vs. 158.4 ± 83.5%, p = 0.010), and lower DEmax (30.8 ± 11.1 mm vs. 40.5 ± 12.5 mm, p = 0.007) compared to stable group. The areas under the TFmax (0.745) and DEmax (0.721) curves indicated fair results for distinguishing exacerbation. The patients were divided into low and high TFmax and DEmax groups based on calculated cut-off values. Low TFmax (odds ratio [OR] 8.40; 95% confidence interval [CI] 1.55–45.56) and low DEmax (OR 11.51; 95% CI 1.15–115.56) were associated with exacerbation after adjusting for age, sex, BMI, forced vital capacity and forced expiratory volume in 1 sec.Conclusion: TFmax and DEmax distinguished exacerbation from stable status. We describe the DUS cut-off values for determining an exacerbation status in this study.

scholarly journals Role of Type2 Inflammatory Biomarkers in Chronic Obstructive Pulmonary Disease

2020 ◽  
Vol 9 (8) ◽  
pp. 2670
Author(s):  
Keiji Oishi ◽  
Kazuto Matsunaga ◽  
Toshihiro Shirai ◽  
Keita Hirai ◽  
Yasuhiro Gon
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Stable State ◽  
Epidemiologic Studies ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Blood Eosinophils ◽  
The Relationship

Airway inflammation in chronic obstructive pulmonary disease (COPD) is typically thought to be driven by Type1 immune responses, while Type2 inflammation appears to be present in definite proportions in the stable state and during exacerbations. In fact, some COPD patients showed gene expression of Type2 inflammation in the airway, and this subset was associated with the inhaled corticosteroid (ICS) response. Interestingly enough, the relationship between COPD and diseases associated with Type2 inflammation from the perspective of impaired lung development is increasingly highlighted by recent epidemiologic studies on the origin of COPD. Therefore, many researchers have shown an interest in the prevalence and the role of existent Type2 biomarkers such as sputum and blood eosinophils, exhaled nitric oxide fraction, and atopy, not only in asthma but also in COPD. Although the evidence about Type2 biomarkers in COPD is inconsistent and less robust, Type2 biomarkers have shown some potential when analyzing various clinical outcomes or therapeutic response to ICS. In this article, we review the existent and emerging Type2 biomarkers with clinically higher applicability in the management of COPD.

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