Biologic Therapy in Chronic Obstructive Pulmonary Disease

Tripple, Julia W.; McCracken, Jennifer; Calhoun, William J.

doi:10.1016/j.iac.2017.01.009

Cited by 6 publications

(5 citation statements)

References 51 publications

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“…The minor criteria include a history of atopy, significant bronchodilator reversibility, and peripheral eosinophilia. Although all COPD patients have not responded to the new biologic agents [74], the ACOS subset may actually benefit.…”

Section: Introductionmentioning

confidence: 99%

Understanding Asthma Phenotypes, Endotypes, and Mechanisms of Disease

Kuruvilla

Lee

2018

Clinic Rev Allerg Immunol

832

719

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The model of asthma as a single entity has now been replaced by a much more complex biological network of distinct and interrelating inflammatory pathways. The term asthma is now considered an umbrella diagnosis for several diseases with distinct mechanistic pathways (endotypes) and variable clinical presentations (phenotypes). The precise definition of these endotypes is central to asthma management due to inherent therapeutic and prognostic implications. This review presents the molecular mechanisms behind the heterogeneity of airway inflammation in asthmatic patients. Asthma endotypes may be broadly regarded as type 2 (T2) high or T2-low. Several biologic agents have been approved for T2-high asthma, with numerous other therapeutics that are incipient and similarly targeted at specific molecular mechanisms. Collectively, these advances have shifted existing paradigms in the approach to asthma to tailor novel therapies.

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Section: Introductionmentioning

confidence: 99%

Understanding Asthma Phenotypes, Endotypes, and Mechanisms of Disease

Kuruvilla

Lee

2018

Clinic Rev Allerg Immunol

832

719

View full text Add to dashboard Cite

show abstract

“…Chronic obstructive pulmonary disease (COPD) is considered the fourth-leading causes of death worldwide, predicted to become the fifth ranked cause of disability worldwide ( 1 ). The development of COPD is caused by inhalation of noxious indoor and outdoor particles ( 2 ), especially cigarette smoke that represents the first risk factor for this respiratory disorder ( 3 ). Herein, chronic inflammatory pattern/s observed in the lung of COPD patients derives from the exposure of both cigarette smoke and air pollution, which affect lung resident and circulating cells ( 1 , 3 , 4 ).…”

Section: Introductionmentioning

confidence: 99%

Chronic Obstructive Pulmonary Disease-Derived Circulating Cells Release IL-18 and IL-33 under Ultrafine Particulate Matter Exposure in a Caspase-1/8-Independent Manner

et al. 2017

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Chronic obstructive pulmonary disease (COPD) is considered the fourth-leading causes of death worldwide; COPD is caused by inhalation of noxious indoor and outdoor particles, especially cigarette smoke that represents the first risk factor for this respiratory disorder. To mimic the effects of particulate matter on COPD, we isolated peripheral blood mononuclear cells (PBMCs) and treated them with combustion-generated ultrafine particles (UFPs) obtained from two different fuel mixtures, namely, pure ethylene and a mixture of ethylene and dimethylfuran (the latter mimicking the combustion of biofuels). UFPs were separated in two fractions: (1) sub-10 nm particles, named nano organic carbon (NOC) particles and (2) primarily soot particles of 20–40 nm and their agglomerates (200 nm). We found that both NOC and soot UFPs induced the release of IL-18 and IL-33 from unstable/exacerbated COPD-derived PBMCs. This effect was associated with higher levels of mitochondrial dysfunction and derived reactive oxygen species, which were higher in PBMCs from unstable COPD patients after combustion-generated UFP exposure. Moreover, lower mRNA expression of the repairing enzyme OGG1 was associated with the higher levels of 8-OH-dG compared with non-smoker and smokers. It was interesting that IL-18 and IL-33 release from PBMCs of unstable COPD patients was not NOD-like receptor 3/caspase-1 or caspase-8-dependent, but rather correlated to caspase-4 release. This effect was not evident in stable COPD-derived PBMCs. Our data suggest that combustion-generated UFPs induce the release of caspase-4-dependent inflammasome from PBMCs of COPD patients compared with healthy subjects, shedding new light into the biology of this key complex in COPD.

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“…Therefore, available antioxidants may modify the inflammatory process in case of many respiratory disorders and protect against the direct detrimental effects of oxidative stress. [5][6][7][8] Constantly produced free radicals can cause damage to healthy cells without protective antioxidative defense. At the same time, free radicals are necessary to maintain health.…”

Section: Reviewmentioning

confidence: 99%

The Key Issues Related to Features and Perspectives of Antioxidants in Asthma and Allergy Pharmacotherapy

Gorgaslidze¹,

Pantsulaia²,

GIORGOBIANI³

et al. 2023

Georgian Biomedical News

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The review aims to highlight the anti-allergenic and anti-inflammatory potential of some antioxidants in the pharmacological treatment of asthma and allergies. Under various physiological and pathological conditions, oxidative stress is both a result of and a contributor to redox metabolism. To effectively manage existing issues, it may be essential to understand the molecular mechanisms of basal oxidative stress and the role of antioxidants. It has been demonstrated that antioxidants can change the biomarkers of allergic inflammation and other consequences of allergy. Antioxidants can neutralize free radicals and control the level of cholesterol and other lipids in the blood. Antioxidants have anticancer activity due to prevention and inhibition of cancer cell growth. Antioxidants stimulate and activate the regeneration of normal, healthy cells. The complexity of each response and the multiple physiological effects complicate clinical studies of antioxidant therapy. Based on the existing evidence, we believe that antioxidants like zeolin-containing Geomin Forte have promising perspectives as adjunctive pharmacotherapy for asthma and allergic diseases.

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Biologic Therapy in Chronic Obstructive Pulmonary Disease

Cited by 6 publications

References 51 publications

Understanding Asthma Phenotypes, Endotypes, and Mechanisms of Disease

Understanding Asthma Phenotypes, Endotypes, and Mechanisms of Disease

Chronic Obstructive Pulmonary Disease-Derived Circulating Cells Release IL-18 and IL-33 under Ultrafine Particulate Matter Exposure in a Caspase-1/8-Independent Manner

The Key Issues Related to Features and Perspectives of Antioxidants in Asthma and Allergy Pharmacotherapy

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