scholarly journals Innate Immune Responses Are Increased in Chronic Obstructive Pulmonary Disease

PLoS ONE ◽  
2011 ◽  
Vol 6 (3) ◽  
pp. e18426 ◽  
Author(s):  
Katherine Joanne Baines ◽  
Jodie Louise Simpson ◽  
Peter Gerard Gibson
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Immune Responses ◽  
Pulmonary Disease ◽  
Innate Immune ◽  
Chronic Obstructive ◽  
Innate Immune Responses ◽  
Obstructive Pulmonary Disease

scholarly journals Biomass smoke as a risk factor for chronic obstructive pulmonary disease: effects on innate immunity

2016 ◽  
Vol 22 (5) ◽  
pp. 373-381 ◽  
Author(s):  
Jordi Olloquequi ◽  
Rafael Silva O
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Innate Immunity ◽  
Risk Factor ◽  
Immune Responses ◽  
Pulmonary Disease ◽  
Innate Immune ◽  
Chronic Obstructive ◽  
Innate Immune Responses ◽  
Obstructive Pulmonary Disease ◽  
Biomass Smoke

Chronic obstructive pulmonary disease (COPD), a major cause of mortality and morbidity worldwide, is considered an archetypical disease of innate immunity, where inhaled particles and gases trigger an inflammatory response, favoring tissue proliferation in small airways and tissue destruction in lung parenchyma, in addition to the recruitment of immune cells to these compartments. Although cigarette smoking is still considered the main risk factor for developing COPD, the trend of proposing biomass smoke (BS) exposure as a principal risk factor is gaining importance, as around 3 billion people worldwide are exposed to this pollutant daily. A considerable amount of evidence has shown the potential of BS as an enhancer of lung inflammation. However, an impairment of some innate immune responses after BS exposure has also been described. Regarding the mechanisms by which biomass smoke alters the innate immune responses, three main classes of cell surface receptors—the TLRs, the scavenger receptors and the transient receptor potential channels—have shown the ability to transduce signals initiated after BS exposure. This article is an updated and comprehensive review of the immunomodulatory effects described after the interaction of BS components with these receptors.

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.

scholarly journals Mitochondrial Regulation of Inflammasome Activation in Chronic Obstructive Pulmonary Disease

2015 ◽  
Vol 8 (2) ◽  
pp. 121-128 ◽  
Author(s):  
Chang Min Yoon ◽  
Milang Nam ◽  
Yeon-Mok Oh ◽  
Charles S. Dela Cruz ◽  
Min-Jong Kang
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Inflammatory Responses ◽  
Pulmonary Inflammation ◽  
Innate Immune ◽  
Western Society ◽  
Future Research ◽  
Chronic Obstructive ◽  
Inflammasome Activation ◽  
Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is characterized by enhanced chronic airway and lung inflammatory responses to noxious particles or gases. It is a major unmet medical need worldwide, and in Western society is strongly associated with exposure to cigarette smoke (CS). CS-induced inflammation is believed to be a key immune driver in the pathogenesis of COPD. Since the concept of inflammasomes was first introduced nearly a decade ago, these have been increasingly recognized as a central player in innate immune and inflammatory responses. In addition, studies have emerged demonstrating that mitochondrial innate immune signaling plays an important role in CS-induced inflammasome activation, pulmonary inflammation and tissue remodeling responses. Here, recent discoveries about inflammasome activation and mitochondrial biology and their role in COPD pathogenesis are reviewed. In addition, the current limitations of our understanding of this theme and future research directions are discussed.

scholarly journals Th17/Treg Imbalance in Chronic Obstructive Pulmonary Disease: Clinical and Experimental Evidence

2021 ◽  
Vol 12 ◽  
Author(s):  
Juliana Dias Lourenço ◽  
Juliana Tiyaki Ito ◽  
Milton de Arruda Martins ◽  
Iolanda de Fátima Lopes Calvo Tibério ◽  
Fernanda Degobbi Tenorio Quirino dos Santos Lopes
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Immune Responses ◽  
Experimental Evidence ◽  
Pulmonary Disease ◽  
Experimental Studies ◽  
Treg Cells ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Anti Inflammatory

The imbalance between pro- and anti-inflammatory immune responses mediated by Th17 and Treg cells is deeply involved in the development and progression of inflammation in chronic obstructive pulmonary disease (COPD). Several clinical and experimental studies have described the Th17/Treg imbalance in COPD progression. Due to its importance, many studies have also evaluated the effect of different treatments targeting Th17/Treg cells. However, discrepant results have been observed among different lung compartments, different COPD stages or local and systemic markers. Thus, the data must be carefully examined. In this context, this review explores and summarizes the recent outcomes of Th17/Treg imbalance in COPD development and progression in clinical, experimental and in vitro studies.

scholarly journals Regulation of lung immunity by dendritic cells: Implications for asthma, chronic obstructive pulmonary disease and infectious disease

2019 ◽  
Vol 25 (6) ◽  
pp. 326-336 ◽  
Author(s):  
Marcus Peters ◽  
Karin Peters ◽  
Albrecht Bufe
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Dendritic Cells ◽  
Immune Responses ◽  
Pulmonary Disease ◽  
Current Knowledge ◽  
Adaptive Immune Response ◽  
Peripheral Tolerance ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
And Control

Since the first description of dendritic cells by Steinman and Cohn in 1973, this important cell type has gained increasing attention. Over 4000 papers have been published on this topic annually during the last few years. At the beginning, dendritic cells were recognized for their immune stimulatory properties and their importance in initiating an adaptive immune response. Later, it was found that dendritic cells do not only initiate but also regulate immune responses. This attribute makes the so-called regulatory dendritic cells highly important for the prevention of exaggerated immune responses. Immune cells make contact with different Ags every day and must be tightly controlled to prevent excessive inflammation and subsequent organ destruction, particularly in organs such as the gut and lungs. Here, we give a brief overview of our current knowledge on how immune responses are controlled by dendritic cells, highlighting how they are involved in the induction of peripheral tolerance. We focus on what is known about these processes in the lung, with a closer look at their role in the induction and control of diseases such as bronchial asthma, chronic obstructive pulmonary disease and lung infections. Finally, we summarize some current approaches to modulate the behavior of dendritic cells that may hopefully lead to future therapeutics to control exaggerated immune responses.

scholarly journals Neutrophilic Inflammation in the Immune Responses of Chronic Obstructive Pulmonary Disease: Lessons from Animal Models

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Gang Huang ◽  
Xu-Chen Xu ◽  
Jie-Sen Zhou ◽  
Zhou-Yang Li ◽  
Hai-Pin Chen ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Animal Models ◽  
Immune Responses ◽  
Pulmonary Disease ◽  
Whole Body ◽  
Chronic Obstructive ◽  
Small Airways ◽  
Obstructive Pulmonary Disease ◽  
Neutrophilic Inflammation ◽  
Advantages And Disadvantages

Chronic obstructive pulmonary disease (COPD) is a major cause of mortality worldwide, which is characterized by chronic bronchitis, destruction of small airways, and enlargement/disorganization of alveoli. It is generally accepted that the neutrophilic airway inflammation observed in the lungs of COPD patients is intrinsically linked to the tissue destruction and alveolar airspace enlargement, leading to disease progression. Animal models play an important role in studying the underlying mechanisms of COPD as they address questions involving integrated whole body responses. This review aims to summarize the current animal models of COPD, focusing on their advantages and disadvantages on immune responses and neutrophilic inflammation. Also, we propose a potential new animal model of COPD, which may mimic the most characteristics of human COPD pathogenesis, including persistent moderate-to-high levels of neutrophilic inflammation.

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