Serum cytokine profiling and enrichment analysis reveal the involvement of immunological and inflammatory pathways in stable patients with chronic obstructive pulmonary disease

Bade, Geetanjali; Khan, Meraj A.; Srivastava, Akhilesh Kumar; Khare, Parul; Solaiappan, Krishna Kumar; Guleria, Randeep; Palaniyar, Nades; Talwar, Anjana

doi:10.2147/copd.s61347

Cited by 24 publications

(17 citation statements)

References 46 publications

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“…Clearly, the lack of a substantial impact of long-term smoking on extracellular IL-16 protein in the blood, as demonstrated in our current study, is in contrast to the corresponding impact on IL-16 protein locally in the airways. 18 – 20 This is also in contrast to a report from Bade et al 43 who showed an increase in serum IL-16 among COPD subjects (current smokers and ex-smokers) compared with nonsmokers and AS. 43 In our study, the COPD group had a decreased gas diffusion capacity, indirectly suggesting emphysema, whereas the AS group, had a normal gas diffusion capacity, arguing against emphysema.…”

Section: Discussioncontrasting

confidence: 93%

Interleukin-16-producing NK cells and T-cells in the blood of tobacco smokers with and without COPD

Andersson¹,

Malmhäll²,

Houltz³

et al. 2016

COPD

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BackgroundLong-term exposure to tobacco smoke causes local inflammation in the airways that involves not only innate immune cells, including NK cells, but also adaptive immune cells such as cytotoxic (CD8+) and helper (CD4+) T-cells. We have previously demonstrated that long-term tobacco smoking increases extracellular concentration of the CD4+-recruiting cytokine interleukin (IL)-16 locally in the airways. Here, we hypothesized that tobacco smoking alters IL-16 biology at the systemic level and that this effect involves oxygen free radicals (OFR).MethodsWe quantified extracellular IL-16 protein (ELISA) and intracellular IL-16 in NK cells, T-cells, B-cells, and monocytes (flow cytometry) in blood samples from long-term tobacco smokers with and without chronic obstructive pulmonary disease (COPD) and in never-smokers. NK cells from healthy blood donors were stimulated with water-soluble tobacco smoke components (cigarette smoke extract) with or without an OFR scavenger (glutathione) in vitro and followed by quantification of IL-16 protein.ResultsThe extracellular concentrations of IL-16 protein in blood did not display any substantial differences between groups. Notably, intracellular IL-16 protein was detected in all types of blood leukocytes. All long-term smokers displayed a decrease in this IL-16 among NK cells, irrespective of COPD status. Further, both NK and CD4+ T-cell concentrations displayed a negative correlation with pack-years. Moreover, cigarette smoke extract caused release of IL-16 protein from NK cells in vitro, and this was not affected by glutathione, in contrast to the decrease in intracellular IL-16, which was prevented by this drug.ConclusionLong-term exposure to tobacco smoke does not markedly alter extracellular concentrations of IL-16 protein in blood. However, it does decrease the intracellular IL-16 concentrations in blood NK cells, the latter effect involving OFR. Thus, long-term tobacco smoking exerts an impact at the systemic level that involves NK cells; innate immune cells that are critical for host defense against viruses and tumors – conditions that are overrepresented among smokers.

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Section: Discussioncontrasting

confidence: 93%

Interleukin-16-producing NK cells and T-cells in the blood of tobacco smokers with and without COPD

Andersson¹,

Malmhäll²,

Houltz³

et al. 2016

COPD

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“…However, the expression of inflammatory factors in emphysematous patients with COPD was slightly higher than that in emphysematous smokers. This result is consistent with the view that smokers with high inflammatory levels are more likely to develop COPD 26 . NE, MMP-9 and MMP-12 are important protease family members, and AAT, SLPI and TIMP-1 plays an important role as an anti-protease 9,27,28 .…”

Section: Discussionsupporting

confidence: 92%

“…Our results showed that the expression of IL-6, IL-10, IL-1β, and TNF-α did not significantly differ between both groups, indicative of comparable inflammatory response. The expression of IL-6 was lower than that of other inflammatory factors, which confirmed that the levels of inflammatory factors in lung tissue are different 26 . However, the expression of inflammatory factors in emphysematous patients with COPD was slightly higher than that in emphysematous smokers.…”

Section: Discussionmentioning

confidence: 56%

Comparative analysis of pathophysiological parameters between emphysematous smokers and emphysematous patients with COPD

Bai

Wang

et al. 2020

Sci Rep

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emphysematous smokers with normal spirometry form a considerable proportion of the clinical population. However, despite presenting with respiratory symptoms and activity limitation, they cannot be diagnosed with chronic obstructive lung disease (copD) according to current criteria. thus, we aimed to determine whether emphysema in smokers has a different pathogenesis from that in patients with COPD. We compared 12 pairs of lung tissue samples from emphysematous patients with normal spirometry and copD, and determined the degree of emphysema using computed tomography. With a focus on COPD-related pathogenesis, we independently assessed inflammatory response, protease-antiprotease balance, oxidative stress, and apoptosis in both groups. Both groups showed similar pathological changes at a comparable degree of emphysema; the expression of inflammatory factors was comparable, with overexpression of proteases and decreased levels of antiproteases. Moreover, there was no significant difference in the activities of glutathione and superoxide dismutase, and expression of apoptosis-related factors. in conclusion, emphysema in smokers with normal spirometry and in patients with COPD had similar pathogenesis. Forced expiratory volume in 1 second cannot be used as the sole diagnostic criterion in patients with copD; early intervention is of great importance to such patients. Chronic obstructive lung disease (COPD) is a chronic respiratory airway disease, with symptoms such as cough, sputum, and shortness of breath 1. The two most prominent pathological changes associated with COPD are the structural destruction of lung tissue and airway remodelling 2. Currently, spirometry is the sole diagnostic criterion for COPD 1,3. Forced expiratory volume in 1 second (FEV1) primarily reflects airflow obstruction and is therefore not suitable for assessing COPD symptoms such as emphysema 4-8. Studies have shown that there is a poor correlation between FEV1 and COPD symptoms 5,6 , as well between FEV1 and the degree of emphysema, as assessed by computed tomography (CT) 7,8. Patients with COPD show high heterogeneity in terms of clinical symptoms, structural destruction, and airway damage 9,10. In some patients, structural destruction of lung tissue is more prominent, and their emphysema severity develops progressively 11. These patients are termed emphysema phenotype of COPD 12,13 , and their structure destruction can be assessed with chest CT scans 14,15. However, chest CT scans have revealed that a considerable number of smokers with obvious emphysema and lung tissue damage show preserved pulmonary function 14-16. According to the current diagnostic criteria, such emphysematous smokers cannot be diagnosed with COPD. If they have same pathogenesis as patients with emphysematous COPD, appropriate interventions to reduce the clinical symptoms and block emphysema progression would be challenging in emphysematous smokers 5,17. In this study, we hypothesized that emphysematous smokers with normal spirometry and emphysematous patients with COP...

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“…[ 2 67 68 69 ] Increased production of such cytokines, indeed, has been demonstrated, and some of them are considered as therapeutic targets of COPD. [ 69 70 71 ] Moreover, systemic inflammation reflected by elevated C-reactive protein (CRP) in the general population has been linked to osteoporosis and to an increased bone resorption. [ 72 73 74 75 76 77 ] Consistent with a role of inflammation in COPD-associated osteoporosis, COPD patients with lower BMD have been shown to have higher levels of CRP and inflammatory cytokines such as TNF-α, IL-1, and IL-6.…”

Section: Disease-specific Risk Factors For Osteoporosis In Copdmentioning

confidence: 99%

Osteoporosis Associated with Chronic Obstructive Pulmonary Disease

2016

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Recent epidemiological studies have revealed that osteoporosis is closely associated with common chronic diseases including diabetes, hypertension, chronic kidney disorders, and chronic obstructive pulmonary disease (COPD). COPD is a chronic inflammatory airway disease but now well known to be associated with various systemic comorbidities including osteoporosis. Osteoporosis and osteoporotic fractures are extremely common in COPD patients, which have significant impacts on their quality of life (QOL), activities of daily life (ADL), respiratory function, and possibly their prognosis. COPD-associated osteoporosis is however extremely under-recognized, hence undertreated. Recent studies have suggested that both decreased bone mineral density (BMD) and impaired bone quality compromise bone strength causing fractures in COPD. In COPD patients, various general clinical risk factors for osteoporosis are present including smoking, older age, low body weight, and physical inactivity. In addition, disease-related risk factors such as decreased pulmonary function, inflammation, glucocorticoid use and vitamin D deficiency/insufficiency have been linked to the development of osteoporosis in COPD. Increased awareness of osteoporosis in COPD, especially that of high prevalence of vertebral fractures is called upon among general physicians as well as pulmonologists. Routine screening for osteoporosis and risk assessment of fractures will enable physicians to diagnose COPD patients with comorbid osteoporosis at an early stage. Timely prevention of developing osteoporosis together with appropriate treatment of established osteoporosis may improve QOL and ADL of the COPD patients, preserve their lung function and eventually result in better prognosis in these patients.

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Serum cytokine profiling and enrichment analysis reveal the involvement of immunological and inflammatory pathways in stable patients with chronic obstructive pulmonary disease

Cited by 24 publications

References 46 publications

Interleukin-16-producing NK cells and T-cells in the blood of tobacco smokers with and without COPD

Interleukin-16-producing NK cells and T-cells in the blood of tobacco smokers with and without COPD

Comparative analysis of pathophysiological parameters between emphysematous smokers and emphysematous patients with COPD

Osteoporosis Associated with Chronic Obstructive Pulmonary Disease

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