2018
DOI: 10.21037/jtd.2018.05.63
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The immune system as a victim and aggressor in chronic obstructive pulmonary disease

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Cited by 15 publications
(10 citation statements)
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“…Alveolar macrophages exposed to long-term tobacco smoke increased IL1A or MCP-1 production, similar to BCG-induced trained macrophages. Promotion of the antimicrobial inflammatory response by these trained macrophages contributes to the exacerbation of chronic obstructive pulmonary disease (COPD) [ 113 ]. Thus, the therapeutic strategies targeting metabolic and epigenetic reprogramming in trained monocytes or macrophages can reverse abnormal macrophages in chronic inflammatory diseases [ 108 ].…”
Section: Innate Immune Memory Of Macrophages In Human Diseasesmentioning
confidence: 99%
“…Alveolar macrophages exposed to long-term tobacco smoke increased IL1A or MCP-1 production, similar to BCG-induced trained macrophages. Promotion of the antimicrobial inflammatory response by these trained macrophages contributes to the exacerbation of chronic obstructive pulmonary disease (COPD) [ 113 ]. Thus, the therapeutic strategies targeting metabolic and epigenetic reprogramming in trained monocytes or macrophages can reverse abnormal macrophages in chronic inflammatory diseases [ 108 ].…”
Section: Innate Immune Memory Of Macrophages In Human Diseasesmentioning
confidence: 99%
“…The therapies explored include phosphodiesterase 4 inhibitors, kinase inhibitors, adenosine A2a-receptor agonists, and agents that interfere with adhesion molecules. [ 35 ] Still, there are concerns about the immune system dysfunction recently found in COPD patients, [ 36 ] because an impaired neutrophilic response may increase the susceptibility to infectious disease.…”
Section: Anti-neutrophilic Inflammatory Strategies For Copdmentioning
confidence: 99%
“…These inflammatory cells release proteolytic enzymes (matrix metalloproteinases, neutrophil elastase) contributing to the destruction of lung tissue, along with TGF-β1 that is involved in the processes of airway remodeling. 13 Using human bronchial cell culture, Pace et al have shown that TLR4/MyD88 signaling plays a key role in the initiation of immune response to exposure to cigarette smoke. The main result of the activation of this signaling pathway is the synthesis of the neutrophil chemoattractant C-X-C Motif Chemokine Ligand 8/interleukin-8 (CXCL8/IL-8).…”
Section: Tlr2 and Tlr4 In The Initiation Of Inflammation In Copdmentioning
confidence: 99%
“…They are involved in the pathogenesis of this disease in several ways. [10][11][12][13] The aim of the review is to analyze the modern views on the role of TLR2 and TLR4 in the pathogenesis of COPD.…”
Section: Introductionmentioning
confidence: 99%