Increased serum IL-17 and decreased serum IL-10 and IL-35 levels correlate with the progression of COPD

Jiang, Shenghua; Zhang, Youwen; Jiang, Luning; Cheng, Zhaozhong

doi:10.2147/copd.s167192

Cited by 40 publications

(35 citation statements)

References 36 publications

(57 reference statements)

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“…As shown in Figure 2, the levels of Th1 (TNF-α), Th2 (IL-17E), and Th17 (IL-17A and IL-22) cell cytokines at admission were significantly higher than those at discharge, and IL-22 and TNF-α exhibited the most significant changes with 2.8-fold and 2.0-fold increases, respectively. IL-10 content was low both during AEs and at the 120-day follow-up, indicating a defective IL-10 response in COPD patients, as previously reported [16]. No significant differences in sputum levels of cytokines were observed among different GOLD stages.…”

Section: Sputum Levels Of T Helper Cell Cytokines During Hospitalizationsupporting

confidence: 80%

“…Studies have shown that high levels of TNF-α and IL-17A are negatively correlated with pulmonary function in COPD [12,15,16]. However, therapies targeting these cytokines (infliximab and etanercept against TNF-α and CNTO 6785 against IL-17) have not shown promising effects in COPD patients, such as an improvement in pulmonary function and symptom scores or a decrease in exacerbations [17][18][19][20][21].…”

mentioning

confidence: 99%

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Th1/Th17 cytokine profiles are associated with disease severity and exacerbation frequency in COPD patients

Zhang

Xie

et al. 2020

Preprint

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Background T helper (Th) cell cytokine imbalances have been associated with the pathophysiology of chronic obstructive pulmonary disease (COPD), including the Th1/Th2 and Th17/Treg paradigms. Clarifying cytokine profiles during COPD acute exacerbation (AE) and their relationships with clinical manifestations would help in understanding the pathogenesis of disease and improve clinical management.Methods Patients admitted to the hospital with AEs of COPD from January 2017 to August 2017 were included in this study, and follow-up was conducted after discharge (every 30 days, for a total of 120 days). Sputum samples of patients at different time points (including at admission, discharge, and follow-up) were collected, and sputum cytokine profiling (12 cytokines in total) was performed using a Luminex assay. Clinical data of patients were collected by a unified electronic medical record form.Results A total of 87 patients with COPD were enrolled, aged 72 ± 8.5 years, among whom 1, 12, 32, and 42 cases exhibited GOLD stage I, II, III, and IV, respectively. According to the cytokine profiles at admission, patients were divided into three clusters by a k -means clustering algorithm, namely, Th1 high Th17 high (n=26), Th1 low Th17 low (n=56), and Th1 high Th17 low (n=5), which revealed distinct clinical characteristics. Patients with Th1 high Th17 low profile had a significantly longer length of non-invasive ventilation time and length of hospital stay than patients with Th1 high Th17 high profile (7 vs. 0 days, 22 vs. 11 days, respectively, p < 0.05), and had the highest AE frequency. Sputum levels of Th17 cytokines (IL-17A, IL-22, and IL-23) during AE were negatively correlated with AE frequency in the last 12 months ( r = -0.258, -0.289 and -0.216, respectively, p < 0.05). Moreover, decreased sputum IL-17A levels were independently associated with increased AE frequency, whith an OR (95% CI) of 0.975 (0.958 - 0.993) and a p = 0.006.Conclusion Th1/Th17 imbalance during AE is associated with the severity of COPD. Decreased Th17 cytokine expression is correlated with increased AE frequency. The Th1/Th17 balance may be a specific target for the therapeutic manipulation of COPD.Trial registration: ClinicalTrials.gov ID: NCT03236480.

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Section: Sputum Levels Of T Helper Cell Cytokines During Hospitalizationsupporting

confidence: 80%

mentioning

confidence: 99%

Th1/Th17 cytokine profiles are associated with disease severity and exacerbation frequency in COPD patients

Zhang

Xie

et al. 2020

Preprint

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“…Several studies have demonstrated similar findings to ours. For example, Jiang et al 53 showed in their study that serum levels of IL-17 were considerably higher in patients with worse severity of disease (stages GOLD III and IV), relating to the progression of the disease. Additionally, Zou et al 54 found that serum IL-1β and IL-17 levels were significantly higher in patients with COPD than in the healthy control group.…”

Section: Discussionmentioning

confidence: 99%

Genetic variants in IL17A and serum levels of IL-17A are associated with COPD related to tobacco smoking and biomass burning

Ponce-Gallegos

Pérez-Rubio

Ambrocio-Ortiz

et al. 2020

Sci Rep

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IL-17A is an important pro-inflammatory cytokine involved in the inflammatory response in chronic obstructive pulmonary disease (COPD). To evaluate the role played by single nucleotide polymorphisms of IL17A and protein levels in susceptibility to COPD, 1,807 subjects were included in a case-control study; 436 had COPD related to tobacco smoking (COPD-S) and 190 had COPD related to biomass burning (COPD-BB). Six hundred fifty-seven smokers without COPD (SWOC) and 183 biomass burningexposed subjects (BBES) served as the respective control groups. The CC genotype and C allele of rs8193036 were associated with COPD (COPD-S vs. SWOC: p < 0.05; OR = 3.01, and OR = 1.28, respectively), as well as a recessive model (p < 0.01; OR = 2.91). Significant differences in serum levels were identified between COPD-S vs. SWOC, COPD-S vs. COPD-BB, and SWOC vs. BBES (p < 0.01). By comparing genotypes in the COPD-BB group TT vs. CC and TC vs. CC (p < 0.05), we found lower levels for the CC genotype. Logistic regression analysis by co-variables was performed, keeping the associations between COPD-S vs. SWOC with both polymorphisms evaluated (p < 0.05), as well as in COPD-BB vs. BBES but with a reduced risk of exacerbation (p < 0.05). In conclusion, polymorphisms in IL17A are associated with COPD. Serum levels of IL-17A were higher in smokers with and without COPD.

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“…68 Moreover, decreased IL-35 levels were negatively correlated with the smoking status, indicating that IL-35 can serve as a biomarker to estimate progression of chronic obstructive pulmonary disease. 69 The above results suggest that IL-35 may be a good indicator of allergic inflammation and can be used as a biomarker.…”

Section: Il-35 and Allergic Airway Diseasementioning

confidence: 81%

“…In addition, studies have shown that the expression of IL‐35 is down‐regulated in chronic obstructive pulmonary disease, a chronic bronchitis and emphysema characterized by airflow obstruction . Moreover, decreased IL‐35 levels were negatively correlated with the smoking status, indicating that IL‐35 can serve as a biomarker to estimate progression of chronic obstructive pulmonary disease . The above results suggest that IL‐35 may be a good indicator of allergic inflammation and can be used as a biomarker.…”

Section: Il‐35 and Immune‐related Diseasesmentioning

confidence: 83%

Interleukin‐35 in immune‐related diseases: protection or destruction

Zhang

Wang

et al. 2019

Immunology

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Summary Interleukin‐35 (IL‐35) is a recently identified heterodimeric cytokine in the IL‐12 family. It consists of an IL‐12 subunit α chain (P35) and IL‐27 subunit Epstein–Barr virus‐induced gene 3 (EBI3) β chain. Unlike the other IL‐12 family members, it signals through four unconventional receptors: IL‐12Rβ2–IL‐27Rα, IL‐12Rβ2–IL‐12Rβ2, IL‐12Rβ2–GP130, and GP130–GP130. Interleukin‐35 signaling is mainly carried out through the signal transducer and activator of transcription family of proteins. It is secreted not only by regulatory T (Treg) cells, but also by CD8+ Treg cells, activated dendritic cells and regulatory B cells. It exhibits immunosuppressive functions distinct from those of other members of the IL‐12 family; these are mediated primarily by the inhibition of T helper type 17 cell differentiation and promotion of Treg cell proliferation. Interleukin‐35 plays a critical role in several immune‐associated diseases, such as autoimmune diseases and viral and bacterial infections, as well as in tumors. In this review, we summarize the structure and function of IL‐35, describe its role in immune‐related disorders, and discuss the mechanisms by which it regulates the development and progression of diseases, including inflammatory bowel disease, collagen‐induced arthritis, allergic airway disease, hepatitis, and tumors. The recent research on IL‐35, combined with improved techniques of studying receptors and signal transduction pathways, allows for consideration of IL‐35 as a novel immunotherapy target.

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Increased serum IL-17 and decreased serum IL-10 and IL-35 levels correlate with the progression of COPD

Cited by 40 publications

References 36 publications

Th1/Th17 cytokine profiles are associated with disease severity and exacerbation frequency in COPD patients

Th1/Th17 cytokine profiles are associated with disease severity and exacerbation frequency in COPD patients

Genetic variants in IL17A and serum levels of IL-17A are associated with COPD related to tobacco smoking and biomass burning

Interleukin‐35 in immune‐related diseases: protection or destruction

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