Role of T-lymphocytes and pro-inflammatory mediators in the pathogenesis of chronic obstructive pulmonary disease

Gadgil, Aneal S.; Duncan, Steven R.

doi:10.2147/copd.s1759

Cited by 57 publications

(15 citation statements)

References 90 publications

(90 reference statements)

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“…Our findings seem to contradict the previously reported increase of CD8 + T-cells and the decrease in CD4 + /CD8 + ratio in smokers compared with never-smokers in BALF and bronchial biopsies [ 13 , 17 – 19 ]. Furthermore, a previous study on bronchial biopsies showed no difference in CD8 + and CD4 + T-lymphocytes before and after smoking cessation [ 26 ].…”

Section: Discussioncontrasting

confidence: 99%

“…The present study did not show any difference in sputum CD4 + T-cell numbers between smokers and never-smokers, as previously shown in [ 8 , 16 , 19 , 26 , 31 ]. Furthermore, no significant changes in the percentages of inflammatory cells (neutrophis, macrophages) in sputum were found in smokers compared to never-smokers.…”

Section: Discussionsupporting

confidence: 89%

“…Moreover, several reports have showed that neutrophils and lymphocytes are increased in smokers [ 6 – 9 , 12 – 16 ]. CD4 + T-cells in BALF of smokers have been reported to be decreased [ 15 , 17 ] and CD8 + T-cells to be increased, resulting in a markedly decreased CD4 + /CD8 + ratio compared to never-smokers [ 18 , 19 ]. Similarly, in the small airway submucosa, there is a trend toward a decrease in CD4 + T-cells, an increase in CD8 + T-cells and a significant decrease in the CD4 + /CD8 + T-cell ratio in smokers as compared to non-smokers [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

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Maintained Smoking Cessation for 6 Months Equilibrates the Percentage of SputumCD8+Lymphocyte Cells with That of Nonsmokers

Bouloukaki

Tsoumakidou

Vardavas

et al. 2009

Mediators of Inflammation

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Little is known about the longitudinal effects of smoking cessation on sputum inflammatory cells. We aimed to investigate the changes in sputum inflammatory cells and T-lymphocyte subpopulations after 6 and 12 months smoking cessation. Induced sputum was obtained from 68 healthy smokers before and after 6 months (n = 21) and 1 year (n = 14) smoking cessation and from ten healthy never-smokers. Inflammatory cells were identified by morphology and T-lymphocyte subpopulations by flow cytometry. Sputum macrophages were decreased after 12 months of smoking cessation in comparison to baseline, while neutrophils increased. Moreover, CD8+ T-cells were decreased in smokers before smoking cessation compared to never-smokers and increased in smokers after 6 months of smoking cessation in comparison to baseline; result that was maintained after 1 year of smoking cessation. These novel findings indicate that smoking cessation can equilibrate certain inflammatory cells of smokers with those of nonsmokers, within 6 months of smoking cessation.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

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Maintained Smoking Cessation for 6 Months Equilibrates the Percentage of SputumCD8+Lymphocyte Cells with That of Nonsmokers

Bouloukaki

Tsoumakidou

Vardavas

et al. 2009

Mediators of Inflammation

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“…CD4 ϩ T cells are responsible for orchestrating immune processes and are critical in amplifying inflammatory responses by other effector immune cells (21). CD4 ϩ T cells can differentiate into distinct effector subsets, including T helper 1 (T H 1), T helper 2 (T H 2), and T helper 17 (T H 17) cells and T regulatory cells (Tregs).…”

mentioning

confidence: 99%

Central role of T helper 17 cells in chronic hypoxia-induced pulmonary hypertension

Maston

Jones

Giermakowska

et al. 2017

American Journal of Physiology-Lung Cellular and Molecular Phys

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Inflammation is a prominent pathological feature in pulmonary arterial hypertension, as demonstrated by pulmonary vascular infiltration of inflammatory cells, including T and B lymphocytes. However, the contribution of the adaptive immune system is not well characterized in pulmonary hypertension caused by chronic hypoxia. CD4 T cells are required for initiating and maintaining inflammation, suggesting that these cells could play an important role in the pathogenesis of hypoxic pulmonary hypertension. Our objective was to test the hypothesis that CD4 T cells, specifically the T helper 17 subset, contribute to chronic hypoxia-induced pulmonary hypertension. We compared indices of pulmonary hypertension resulting from chronic hypoxia (3 wk) in wild-type mice and recombination-activating gene 1 knockout mice (RAG1, lacking mature T and B cells). Separate sets of mice were adoptively transferred with CD4, CD8, or T helper 17 cells before normoxic or chronic hypoxic exposure to evaluate the involvement of specific T cell subsets. RAG1 mice had diminished right ventricular systolic pressure and arterial remodeling compared with wild-type mice exposed to chronic hypoxia. Adoptive transfer of CD4 but not CD8 T cells restored the hypertensive phenotype in RAG1 mice. Interestingly, RAG1 mice receiving T helper 17 cells displayed evidence of pulmonary hypertension independent of chronic hypoxia. Supporting our hypothesis, depletion of CD4 cells or treatment with SR1001, an inhibitor of T helper 17 cell development, prevented increased pressure and remodeling responses to chronic hypoxia. We conclude that T helper 17 cells play a key role in the development of chronic hypoxia-induced pulmonary hypertension.

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“…Pathogenic T cells are also important in the orchestration and perpetuation of the inflammatory damages in a context of COPD. The frequency of both CD4 ϩ T cells secreting T-helper (Th)-1 (19), Th-2 (35), or Th-17 (7) cytokines and CD8 ϩ T-cytotoxic (Tc) cells producing interferon-␥ (IFN-␥) (16) in various biological fluids correlates with activity and severity of the disease in patients with COPD. We previously demonstrated that instillation of EP to mice resulted in an acute emphysematous state (37) associated with a Th-1, Th-17, and Tc-1 proinflammatory response (31).…”

Section: Introductionmentioning

confidence: 99%

Impact of aging on inflammatory and immune responses during elastin peptide-induced murine emphysema

Pierre

Lemaire

Meghraoui-Kheddar

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

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Deterioration of lung functions and degradation of elastin fibers with age are accelerated during chronic obstructive pulmonary disease (COPD). Excessive genesis of soluble elastin peptides (EP) is a key factor in the pathophysiology of COPD. We have previously demonstrated that 6-wk-old mice exhibited emphysematous structural changes associated with proinflammatory immune response after EP instillation. In this study, we investigated the consequences of aging on inflammatory, immune, and histological criteria associated with murine emphysema progression after EP exposure. Young (6 wk old) and elderly (15 mo old) C57BL/6J mice were endotracheally instilled with EP, and, at various time points after treatment, the inflammatory cell profiles from bronchoalveolar lavage fluids (BALF) and the T-lymphocyte phenotypes, at local and systemic levels, were analyzed by flow cytometry. Lungs were also prepared to allow morphological and histological analysis by confocal microscopy. Elderly mice exhibited an earlier development of pulmonary emphysema, characterized by an increase of the inflammatory and lymphocytic infiltrates, extracellular matrix breakdown, and airspace enlargement compared with young mice. This age-dependent parenchymal tissue remodeling was associated with an increase of the matrix metalloproteinase expressions and desmosine levels in BALF and/or sera of EP-treated mice. In addition, both the proportion of CD4+CD28− and CD8+CD28− T cells in the tissues of EP-treated mice and the interferon-γ levels in the EP-specific memory T-cell clones were significantly higher in elderly versus younger mice. This study demonstrates that aging accelerates emphysema development and that this effect is linked to increased EP production and their effects on inflammatory and immune response.

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Role of T-lymphocytes and pro-inflammatory mediators in the pathogenesis of chronic obstructive pulmonary disease

Cited by 57 publications

References 90 publications

Maintained Smoking Cessation for 6 Months Equilibrates the Percentage of SputumCD8+Lymphocyte Cells with That of Nonsmokers

Maintained Smoking Cessation for 6 Months Equilibrates the Percentage of SputumCD8+Lymphocyte Cells with That of Nonsmokers

Central role of T helper 17 cells in chronic hypoxia-induced pulmonary hypertension

Impact of aging on inflammatory and immune responses during elastin peptide-induced murine emphysema

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