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

@article{DeFalco2017ChronicOP,
  title={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},
  author={Gianluigi De Falco and Chiara Colarusso and Michela Terlizzi and Ada Popolo and Michela Pecoraro and Mario Commodo and Patrizia Minutolo and Mariano Sirignano and Andrea D’Anna and Rita Aquino and Aldo Pinto and Antonio Molino and Rosalinda Sorrentino},
  journal={Frontiers in Immunology},
  year={2017},
  volume={8}
}
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… 
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26 Citations
Background Citations
5
Methods Citations
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26 Citations

AIM2 Inflammasome Activation Leads to IL-1α and TGF-β Release From Exacerbated Chronic Obstructive Pulmonary Disease-Derived Peripheral Blood Mononuclear Cells
TLDR
Interestingly, AIM2-depedent IL-1α release was responsible for higher TGF-β levels, crucial mediator during pro-fibrotic processes associated to COPD progression, opening new therapeutic perspectives for unstable COPD patients.
AIM2/IL-1α/TGF-β Axis in PBMCs From Exacerbated Chronic Obstructive Pulmonary Disease (COPD) Patients Is Not Related to COX-2-Dependent Inflammatory Pathway
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Evaluating the activity of Absent in melanoma 2 (AIM2) inflammasome-dependent pathways under corticosteroid treatment during COPD exacerbation found that IL-1α was highly increased when AIM2 was activated from Poly dA:dT in exacerbated, but not in stable, COPD-derived PBMCs.
The Inhibition of Caspase-1- Does Not Revert Particulate Matter (PM)-Induced Lung Immunesuppression in Mice
TLDR
This study proves that PM exposure leads to an immunosuppressive lung environment in a caspase-1-independent manner, paving the way to understand the molecular and cellular mechanism/s underlying the establishment of some respiratory disorders according to the exposure to air pollution.
Polyphenols, flavonoids and inflammasomes: the role of cigarette smoke in COPD.
TLDR
The known associations between inflammasome-mediated responses and ameliorations in pre-clinical manifestations of CS-COPD via polyphenol and flavonoid treatment are reviewed, with a focus on the underlying mechanistic insights.
Variations in Reactive Oxygen Species Generation by Urban Airborne Particulate Matter in Lung Epithelial Cells—Impact of Inorganic Fraction
TLDR
The influence of airborne particulate matter and their inorganic components on biological function of human alveolar-like epithelial cells was investigated in vitro and the difference in the reactive oxygen species (ROS) profiles generated by organic and inorganic counterparts of PM was shown.
Caspase-11 and AIM2 inflammasome are involved in smoking-induced COPD and lung adenocarcinoma
TLDR
It is found that AIM2 inflammasome is at the crossroad between COPD and lung cancer in that its higher presence is correlated to lower survival rate of smoking COPD adenocarcinoma patients.
Chronic Obstructive Pulmonary Disease COPD and lung cancer: is the inflammasome at the cross talk?
TLDR
The data support the role of the inflammasome in both COPD and lung cancer establishment and found that absent in melanoma 2 (AIM2) inflammaome paves the way for chronic inflammatory conditions at the basis of both COPd and NSCLC, standing at the crossroad for lung carcinogenesis.
New Insights into the Implication of Mitochondrial Dysfunction in Tissue, Peripheral Blood Mononuclear Cells, and Platelets during Lung Diseases
TLDR
It is shown that circulating blood cells mitochondrial oxidative capacity are likely to be reduced in chronic obstructive pulmonary disease (COPD), but enhanced in asthma and pulmonary arterial hypertension in a context of increased oxidative stress.
Angiogenesis, Lymphangiogenesis, and Inflammation in Chronic Obstructive Pulmonary Disease (COPD): Few Certainties and Many Outstanding Questions
TLDR
Although there is evidence that alterations of angiogenesis and, to a lesser extent, lymphangiogenesis, are associated with COPD, there are still many unanswered questions.
IL-33 in Chronic Respiratory Disease: From Preclinical to Clinical Studies.
TLDR
Key clinical evidence for the potential of targeting increased IL-33 in respiratory diseases including exacerbations is highlighted, and current clinical trials using an anti-IL-33 monoclonal antibody in asthma patients are outlined.
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