scholarly journals Human Rhinovirus Impairs the Innate Immune Response to Bacteria in Alveolar Macrophages in Chronic Obstructive Pulmonary Disease

2019 ◽  
Vol 199 (12) ◽  
pp. 1496-1507 ◽  
Author(s):  
Lydia J. Finney ◽  
Kylie B. R. Belchamber ◽  
Peter S. Fenwick ◽  
Samuel V. Kemp ◽  
Michael R. Edwards ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Immune Response ◽  
Pulmonary Disease ◽  
Innate Immune Response ◽  
Alveolar Macrophages ◽  
Innate Immune ◽  
Human Rhinovirus ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Peripheral compartment innate immune response toHaemophilus influenzaeandStreptococcus pneumoniaein chronic obstructive pulmonary disease patients

2012 ◽  
Vol 19 (4) ◽  
pp. 428-437 ◽  
Author(s):  
Santiyagu M Savarimuthu Francis ◽  
Maxine E Tan ◽  
Pamela R Fung ◽  
Janet G Shaw ◽  
Annalese BT Semmler ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Immune Response ◽  
Pulmonary Disease ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Peripheral Compartment ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

scholarly journals Epilobiumpyrricholophum Extract Suppresses Porcine Pancreatic Elastase and Cigarette Smoke Extract-Induced Inflammatory response in a Chronic Obstructive Pulmonary Disease Model

Foods ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 2929
Author(s):  
Sun Young Jung ◽  
Gun-Dong Kim ◽  
Dae Woon Choi ◽  
Dong-Uk Shin ◽  
Ji-Eun Eom ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Obstructive Pulmonary Disease ◽  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Inflammatory Gene Expression ◽  
Pancreatic Elastase ◽  
Porcine Pancreatic Elastase

Chronic airway exposure to harmful substances, such as deleterious gases, cigarette smoke (CS), and particulate matter, triggers chronic obstructive pulmonary disease (COPD), characterized by impaired lung function and unbridled immune responses. Emerging epigenomic and genomic evidence suggests that excessive recruitment of alveolar macrophages and neutrophils contributes to COPD pathogenesis by producing various inflammatory mediators, such as reactive oxygen species (ROS), neutrophil elastase, interleukin (IL) 6, and IL8. Recent studies showed that Epilobium species attenuated ROS, myeloperoxidase, and inflammatory cytokine production in murine and human innate immune cells. Although the Epilobium genus exerts anti-inflammatory, antioxidant, and antimicrobial effects, the question of whether the Epilobium species regulate lung inflammation and innate immune response in COPD has not been investigated. In this study, Epilobium pyrricholophum extract (EPE) suppressed inflammatory cell recruitment and clinical symptoms in porcine pancreatic elastase and CS extract-induced COPD mice. In addition, EPE attenuated inflammatory gene expression by suppressing MAPKs and NFκB activity. Furthermore, UPLC-Q-TOF MS analyses revealed the anti-inflammatory effects of the identified phytochemical constituents of EPE. Collectively, our studies revealed that EPE represses the innate immune response and inflammatory gene expression in COPD pathogenesis in mice. These findings provide insights into new therapeutic approaches for treating COPD.

scholarly journals Orchestration of Neutrophil Extracellular Traps (Nets), a Unique Innate Immune Function during Chronic Obstructive Pulmonary Disease (COPD) Development

Biomedicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 53
Author(s):  
Anjali Trivedi ◽  
Meraj A. Khan ◽  
Geetanjali Bade ◽  
Anjana Talwar
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Neutrophil Extracellular Traps ◽  
Innate Immune ◽  
Chronic Obstructive ◽  
Tissue Destruction ◽  
Mucus Production ◽  
Obstructive Pulmonary Disease ◽  
Extracellular Traps ◽  
Endothelial Cell Death

Morbidity, mortality and economic burden caused by chronic obstructive pulmonary disease (COPD) is a significant global concern. Surprisingly, COPD is already the third leading cause of death worldwide, something that WHO had not predicted to occur until 2030. It is characterized by persistent respiratory symptoms and airway limitation due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles of gases. Neutrophil is one of the key infiltrated innate immune cells in the lung during the pathogenesis of COPD. Neutrophils during pathogenic attack or injury decide to undergo for a suicidal death by releasing decondensed chromatin entangled with antimicrobial peptides to trap and ensnare pathogens. Casting neutrophil extracellular traps (NETs) has been widely demonstrated to be an effective mechanism against invading microorganisms thus controlling overwhelming infections. However, aberrant and massive NETs formation has been reported in several pulmonary diseases, including chronic obstructive pulmonary disease. Moreover, NETs can directly induce epithelial and endothelial cell death resulting in impairing pulmonary function and accelerating the progression of the disease. Therefore, understanding the regulatory mechanism of NET formation is the need of the hour in order to use NETs for beneficial purpose and controlling their involvement in disease exacerbation. For example, DNA neutralization of NET proteins using protease inhibitors and disintegration with recombinant human DNase would be helpful in controlling excess NETs. Targeting CXC chemokine receptor 2 (CXCR2) would also reduce neutrophilic inflammation, mucus production and neutrophil-proteinase mediated tissue destruction in lung. In this review, we discuss the interplay of NETs in the development and pathophysiology of COPD and how these NETs associated therapies could be leveraged to disrupt NETopathic inflammation as observed in COPD, for better management of the disease.

Sign in / Sign up

Export Citation Format

Share Document