scholarly journals IL-17 Aggravates Pseudomonas aeruginosa Airway Infection in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

2022 ◽  
Vol 12 ◽  
Author(s):  
Fengming Ding ◽  
Lei Han ◽  
Qiang Fu ◽  
Xinxin Fan ◽  
Rong Tang ◽  
...  
Keyword(s):  
Mouse Models ◽  
Inflammatory Cytokine ◽  
Inflammatory Responses ◽  
Neutralizing Antibody ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Airway Infection ◽  
Copd Patients ◽  
Acute Exacerbations

Pseudomonas aeruginosa airway infection increases risks of exacerbations and mortality in chronic obstructive pulmonary disease (COPD). We aimed to elucidate the role of IL-17 in the pathogenesis. We examined the expression and influences of IL-23/IL-17A in patients with stable COPD (n = 33) or acute COPD exacerbations with P. aeruginosa infection (n = 34). A mouse model of COPD (C57BL/6) was used to investigate the role of IL-17A in host inflammatory responses against P. aeruginosa infection through the application of IL-17A–neutralizing antibody or recombinant IL-17A. We found that P. aeruginosa infection increased IL-23/17A signaling in lungs of both COPD patients and COPD mouse models. When COPD mouse models were treated with neutralizing antibody targeting IL-17A, P. aeruginosa induced a significantly less polymorphonuclear leukocyte infiltration and less bacterial burden in their lungs compared to those of untreated counterparts. The lung function was also improved by neutralizing antibody. Furthermore, IL-17A-signaling blockade significantly reduced the expression of pro-inflammatory cytokine IL-1β, IL-18, TNF-α, CXCL1, CXCL15 and MMP-9, and increased the expression of anti-inflammatory cytokine IL-10 and IL-1Ra. The application of mouse recombinant IL-17A exacerbated P. aeruginosa-mediated inflammatory responses and pulmonary dysfunction in COPD mouse models. A cytokine protein array revealed that the expression of retinol binding protein 4 (RBP4) was down-regulated by IL-17A, and exogenous RBP4-recombinant protein resulted in a decrease in the severity of P. aeruginosa-induced airway dysfunction. Concurrent application of IL-17A-neutralizing antibody and ciprofloxacin attenuated airway inflammation and ventilation after inoculation of P. aeruginosa in COPD mouse models. Our results revealed that IL-17 plays a detrimental role in the pathogenesis of P. aeruginosa airway infection during acute exacerbations of COPD. Targeting IL-17A is a potential therapeutic strategy in controlling the outcomes of P. aeruginosa infection in COPD patients.

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.

Role of the Management Pathway in the Care of Advanced COPD Patients in Their Own Homes

2010 ◽  
Vol 11 (4) ◽  
pp. 249-253 ◽  
Author(s):  
Ashok A. Ramani ◽  
Anthony A. Pickston ◽  
James L. Clark ◽  
Courtney A. Clark ◽  
Michael Brown
Keyword(s):  
Home Visits ◽  
Cost Benefit ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Respiratory Therapists ◽  
The Third ◽  
Home Based ◽  
Copd Patients ◽  
Home Based Intervention

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide, and the incidence and prevalence are rising every decade. The cost of hospital admission is substantial and is the single largest source of expenditure in care of COPD patients. Home-based intervention has been shown to provide long-term cost benefit in a range of chronic illnesses; however, the role of home visits by respiratory therapists (RT) in COPD management has not been evaluated. The aim of this study was to assess the effectiveness of a management pathway in the care of oxygen dependent COPD patients in their homes. Oxygen-dependent COPD patients were enrolled in the management pathway after discharge from the hospital or referred from a provider’s office. At least three home visits were made: the first within 3 days of enrollment, the second in 1 month, and the third 10 months later. Three hundred and twenty-four patients were enrolled in the study. During the study period, the overall hospitalization rate dropped (11% per month at the second visit vs. 2.1% per month at the third visit). The patients’ understanding of the disease improved substantially (21.6% vs. 83.9%), knowledge of medications the patients were taking improved (56.0% vs. 87.0%), and appropriate use of medications increased (52.0% vs. 86.0%). In our community, this RT-led program helped patients’ self-management of COPD in their own homes by increasing understanding of the disease, assisted physicians in monitoring their patients, and reduced hospitalization.

scholarly journals Protective Features of Autophagy in Pulmonary Infection and Inflammatory Diseases

Cells ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 123 ◽  
Author(s):  
Kui Wang ◽  
Yi Chen ◽  
Pengju Zhang ◽  
Ping Lin ◽  
Na Xie ◽  
...  
Keyword(s):  
Pulmonary Infection ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Autophagy Pathway ◽  
Pulmonary Arterial ◽  
Cellular Components ◽  
Cellular Stressors

Autophagy is a highly conserved catabolic process involving autolysosomal degradation of cellular components, including protein aggregates, damaged organelles (such as mitochondria, endoplasmic reticulum, and others), as well as various pathogens. Thus, the autophagy pathway represents a major adaptive response for the maintenance of cellular and tissue homeostasis in response to numerous cellular stressors. A growing body of evidence suggests that autophagy is closely associated with diverse human diseases. Specifically, acute lung injury (ALI) and inflammatory responses caused by bacterial infection or xenobiotic inhalation (e.g., chlorine and cigarette smoke) have been reported to involve a spectrum of alterations in autophagy phenotypes. The role of autophagy in pulmonary infection and inflammatory diseases could be protective or harmful dependent on the conditions. In this review, we describe recent advances regarding the protective features of autophagy in pulmonary diseases, with a focus on ALI, idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD), tuberculosis, pulmonary arterial hypertension (PAH) and cystic fibrosis.

scholarly journals The Mechanisms of Benefit of High-Flow Nasal Therapy in Stable COPD

2020 ◽  
Vol 9 (12) ◽  
pp. 3832
Author(s):  
Massa Zantah ◽  
Aloknath Pandya ◽  
Michael R. Jacobs ◽  
Gerard J. Criner
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Mucociliary Clearance ◽  
High Flow ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Flow Rates ◽  
Copd Patients ◽  
Unique System ◽  
Co2 Washout

High-flow nasal therapy (HFNT) is a unique system that delivers humidified, heated oxygen-enriched air via nasal cannula at high flow rates. It is a promising therapy for chronic obstructive pulmonary disease (COPD) patients. Several studies have examined the physiologic effects of this therapy in the patient population and have revealed that it improves mucociliary clearance, reduces nasopharyngeal dead space, and subsequently increases CO2 washout. It also improves alveolar recruitment and gas exchange. These mechanisms may explain the promising results observed in recently published studies that examined the role of HFNT in stable COPD patients.

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