Update in Chronic Obstructive Pulmonary Disease 2007

MacNee, William

doi:10.1164/rccm.200801-167up

Cited by 14 publications

(4 citation statements)

References 205 publications

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“…Given current clinical practice in the treatment of COPD, it should be emphasized that our study forwards no evidence that treatment with a glucocorticoid receptor agonist and/or a ␤-adrenoreceptor agonist can prevent the IL-16 release caused by the water-soluble components of tobacco smoke in human CD8 ϩ cells. These experimental observations are also compatible with the clinical experience that neither of these drug classes has been proven to substantially alter the clinical progression of COPD (6,23,30).…”

Section: Discussionsupporting

confidence: 85%

Effects of tobacco smoke on IL-16 in CD8⁺ cells from human airways and blood: a key role for oxygen free radicals?

Andersson¹,

Bossios

Malmhäll

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

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Chronic exposure to tobacco smoke leads to an increase in the frequency of infections and in the number of CD8(+) and CD4(+) cells as well as the CD4(+) chemoattractant cytokine IL-16 in the airways. Here, we investigated whether tobacco smoke depletes intracellular IL-16 protein and inhibits de novo production of IL-16 in CD8(+) cells from human airways and blood while increasing extracellular IL-16 and whether oxygen free radicals (OFR) are involved. Intracellular IL-16 protein in CD8(+) cells and mRNA in all cells was decreased in bronchoalveolar lavage (BAL) samples from chronic smokers. This was also the case in human blood CD8(+) cells exposed to water-soluble tobacco smoke components in vitro, in which oxidized proteins were markedly increased. Extracellular IL-16 protein was increased in cell-free BAL fluid from chronic smokers and in human blood CD8(+) cells exposed to water-soluble tobacco smoke components in vitro. This was not observed in occasional smokers after short-term exposure to tobacco smoke. A marker of activation (CD69) was slightly increased, whereas other markers of key cellular functions (membrane integrity, apoptosis, and proliferation) in human blood CD8(+) cells in vitro were negatively affected by water-soluble tobacco smoke components. An OFR scavenger prevented these effects, whereas a protein synthesis inhibitor, a β-adrenoceptor, a glucocorticoid receptor agonist, a phosphodiesterase, a calcineurin phosphatase, and a caspase-3 inhibitor did not. In conclusion, tobacco smoke depletes preformed intracellular IL-16 protein, inhibits its de novo synthesis, and distorts key cellular functions in human CD8(+) cells. OFR may play a key role in this context.

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Section: Discussionsupporting

confidence: 85%

Effects of tobacco smoke on IL-16 in CD8⁺ cells from human airways and blood: a key role for oxygen free radicals?

Andersson¹,

Bossios

Malmhäll

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Most of IL-17a is secreted by memory T cells during the induction of inflammatory responses. 32 , 33 In the lungs, IL-17a plays a key role in the onset of COPD by stimulating the growth of fibroblasts and endothelial cells in the airways. IL-17a can also promote the secretion of IL-6 and IL-8 to impair lung tissues in the onset of COPD and chronic airway inflammation.…”

Section: Discussionmentioning

confidence: 99%

Microbiota Imbalance Contributes to COPD Deterioration by Enhancing IL-17a Production via miR-122 and miR-30a

Zhu

Zhou

Xu³

et al. 2020

Molecular Therapy - Nucleic Acids

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The changes of microbiota in lungs could change interleukin-17a (IL-17a) expression by altering microRNAs (miRNAs) profile, thus contributing to the pathogenesis of chronic obstructive pulmonary disease (COPD). In this study, we aimed to study molecular mechanisms’ underlying effect of microbiota imbalance on COPD deterioration. Real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) were performed to analyze expression of miRNAs and IL-17a mRNA. ELISA was used to evaluate abundance of IL-17a in plasma, peripheral blood monocyte, and sputum of COPD mice and patients. Luciferase assay was performed to explore underlying molecular mechanisms. The expression of miR-122, miR-30a, and miR-99b were remarkably decreased in COPD mice, while the expression of IL-17a was notably increased in plasma, peripheral blood monocytes, and lung tissues of COPD mice. The levels of Lactobacillus/Moraxella and IL-17a expression were significantly enhanced in sputum of exacerbated COPD patients, along with notably decreased expression of miR-122 and miR-30a. Luciferase assay confirmed that miR-122 and miR-30a played an inhibitory role in IL-17a expression. We identified miR-122 and miR-30a as differentially expressed miRNAs in sputum and plasma of COPD patients in exacerbation-month12 group. Furthermore, downregulated miR-122 and miR-30a expression associated with microbiota imbalance may contribute to COPD deterioration by enhancing IL-17a production.

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“…Several candidate genes are found to contribute to the individual risk. Environmental risk factors include smoking as the first cause followed by air pollution and occupational dust or chemicals [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Novel autoantigens immunogenic in COPD patients

et al. 2009

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Update in Chronic Obstructive Pulmonary Disease 2007

Cited by 14 publications

References 205 publications

Effects of tobacco smoke on IL-16 in CD8⁺ cells from human airways and blood: a key role for oxygen free radicals?

Effects of tobacco smoke on IL-16 in CD8⁺ cells from human airways and blood: a key role for oxygen free radicals?

Microbiota Imbalance Contributes to COPD Deterioration by Enhancing IL-17a Production via miR-122 and miR-30a

Novel autoantigens immunogenic in COPD patients

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Update in Chronic Obstructive Pulmonary Disease 2007

Cited by 14 publications

References 205 publications

Effects of tobacco smoke on IL-16 in CD8+ cells from human airways and blood: a key role for oxygen free radicals?

Effects of tobacco smoke on IL-16 in CD8+ cells from human airways and blood: a key role for oxygen free radicals?

Microbiota Imbalance Contributes to COPD Deterioration by Enhancing IL-17a Production via miR-122 and miR-30a

Novel autoantigens immunogenic in COPD patients

Contact Info

Product

Resources

About

Effects of tobacco smoke on IL-16 in CD8⁺ cells from human airways and blood: a key role for oxygen free radicals?

Effects of tobacco smoke on IL-16 in CD8⁺ cells from human airways and blood: a key role for oxygen free radicals?