Influence of inflammatory cytokines on the course of chronic obstructive pulmonary disease

  • Received 17.12.2020

  • Revised 20.01.2021

  • Accepted 23.02.2021



  • 1,026 Views

  • Retrieved from Volume 3, No. 1, 2021

  • Pages 46-53

Summary. Chronic obstructive pulmonary disease (COPD) is one of the leading health problems worldwide, due to the high prevalence of this pathology, fairly high rates of disability and mortality, as well as large economic losses. This disease is the most common cause of disability and mortality among all lung diseases. According to experts, in 2020, mortality from COPD should have come in third place. The aim of the study – to learn the effect of inflammatory cytokines on the course of chronic obstructive pulmonary disease (COPD). Materials and Methods: The total number of exa­mined patients was 146 people, who were compared by age and sex. Group 1 consisted of 100 patients with COPD (38 patients had stage II bronchoobstruction, stage III – 43 patients, stage IV – 19 patients). Group 2 consisted of relatively healthy smokers with smoking experience ≥ 10 packs/year (24 people). Group 3 consisted of healthy non-smoking men with smoking experience ≤ 1 pack/year (22 people). Patients underwent spirometric examination; blood test for biomarkers of inflammation (BI), namely leukocytes, C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-8 (IL-8), fibrinogen; computed tomography of the lungs; body mass index (BMI) measurements; mMRC test, SGRQ and CAT questionnaires. The level of BI in patients with COPD was compared with those in healthy smokers with normal spirometry and non-smokers. Kraskel-Wallis tests were used to analyze the statistical significance of differences between groups. Significance of differences between quantitative traits with abnormal distribution was performed using the nonparametric pair U Mann-Whitney test. Comparison of qualitative indicators was performed using the criterion χ2 with Yates correction. In all cases, differences at p <0.05 were considered significant. Results. The results showed that the level of BI, namely leukocytes, CRP, IL-6 and fibrinogen is statistically higher (p <0.001) in patients with COPD than in smokers with normal lung function and non-smokers, while the level of IL-8 is higher in the group of smokers without COPD (p <0,001). The mean levels of CRP, IL-6, and fibrinogen were almost indistinguishable between smokers and ex-smokers within the study groups, whereas the level of IL-8 in current smokers was statistically higher than in those who quit smoking as in patients with COPD (p <0.01) and in the group of smokers with normal spirometry (p <0.001). The percentage of people with elevated levels of BI was significantly higher in group 1 compared to group 2 (70 % and 62 %, respectively, p <0.05) and in group 2 compared to group 3 (62 % and 22 %, respectively, p <0.001). The percentage of patients who had an increase in 2 or more BI was also statistically higher in the group of COPD compared with smokers without COPD (p <0.05) and non-smokers (p <0.001). There is a direct correlation between the severity of BI and bronchoobstruction of COPD (r = 0.39, p <0.05). In patients with COPD, there were direct positive correlations between the severity of BI and smoking experience (r = 0.82; p <0.05), the severity of shortness of breath on the mMRC scale (r = 0.62; p <0.05), the presence of concomitant pathology (r = 0.51; p <0.05), the frequency of pulmonary emphysema and exacerbations during the year (r = 0.82 and r = 0.89, respectively; p <0.05). Conclusions. The obtained results allow us to consider BI in patients with COPD as a factor that modifies the development of pathology

chronic obstructive pulmonary disease, biomarkers of inflammation, cytokines, systemic inflammation, body mass index

https://doi.org/10.11603/bmbr.2706-6290.2021.1.12087

[1] Feschenko  YuI.  [Bronchial  asthma,  chronic obstructive pulmonary disease: a promising global strategy, the  latest  diagnostic  methods,  modern  approaches  to therapy] Astma ta alergiya. 2015;4: 38-42. Ukrainian.

[2] Ospanova TS, Semidotskaya ZhD, Chernyakova IA, Pionova  EN,  Trifonova  NS.  [The  COPD  phenotype  – the  path  to  personalized  medicine  of  the  XXI  century]. Shidnoevropeyskyi   zhurnal   vnutrishnoi   ta   simeinoi medytsyny. Pulmonolohiia. 2017;1: 95-101. Ukrainian.

[3] Feschenko YuI, Yashina LO, Dzyublik OYa. [Chronic obstructive pulmonary disease: etiology, pathogenesis, classification, diagnosis, therapy (draft national agreement) material  congress].  Ukrainskyi  pulmonolohichnyi  zhurnal. 2013;3: 7-12. Ukrainian.

[4] Zhang M, Wan Y, Jin Y, Xin JB, Zhang JC, Xiong XZ, et al. Cigarette smoking promotes inflammation in patients with  COPD  by  affecting  the  polarization  and  survival  of Th/Tregs  through  up-regulation  of  muscarinic  receptor. PLoS  ONE.  2014;9(11):  e112350.  DOI:  10.1371/journal.pone.0112350

[5] Aysanov  ZR,  Chernyak  AV,  Kalmanova  EN. [Spirometry for diagnosis and therapeutic efficacy evaluation in chronic obstructive pulmonary disease in primary care]. Ros pulmonol. 2014;(5): 101-10. Available from: https://doi.org/10.18093/0869-0189-2014-0-5-101-110. Russian.

[6] Pogrebnyak  OO.  [Review  of  current  guidelines for  the  management  of  patients  with  chronic  obstructive pulmonary  disease:  the  results  of  the  International Congress  "Prevention.  Anti-aging’’]. Liky  Ukrainy.  2015;7 (193). Ukrainian.

[7] Singh D, Agusti A, Anzueto A, Barnes PJ, Bourbeau J, Celli  BR,  et  al.  Global  strategy  for  prevention,  diagnosis and  management  of  COPD  2019.  Eur  Respir  J.  2019. DOI:10.1183/13993003.00164-2019

[8] Dudka PF, Dobryanskiy DV, Ilnitsky RI. [Hemoreological and immune disorders and the possibility of their correction in  patients  with  chronic  obstructive  pulmonary  fixation]. Molodyi  vchenyi.  2014;2(05):  157-160.  Available  from: http://nbuv.gov.ua/UJRN/molv_2014_2(05)__39. Ukrainian.

[9] Vanfleteren LE, Spruit MA, Groenen M, Gaffron S, van Empel VP, Bruijnzeel PL, et al. Clusters of comorbidities based on validated objective measurements and systemic inflammation in patients with chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine. 2013;7: 728-35.

[10] Kochubey  OA.  [Cytokines,  as  primary  mediators in  the  regulation  of  the  reaction  of  inflammation]. General  Therapeutic  Practice:  New  Technologies  and Interdisciplinary Issues, materials of the scientific-practical conference with international participation. Kharkiv; 2013. Ukrainian.

[11] Mamaeva MG, Demko IV, Verigo YaI, Kraposhina AYu, Solovieva  IA,  Hendogina  VT.  [Markers  of  systemic inflammation  and  endothelial  dysfunction  in  chronic obstructive  pulmonary  disease]  Sibirskoe  meditsinskoe obrazovanie. 2014;1: 12-9. Russian.

[12] Matvienko YuO. [Biomarkers and their place in the pathogenesis  of  chronic  obstructive  pulmonary  disease]. Astma ta alerhiia. 2016;3: 1-6. Ukrainian.

[13] Gumeniuk  MI,  Ignatieva  VI,  Matviienko  YuA, Iliinska IF, Harchenko-Sevrukova GS. [Markers of systemic inflammation in patients with chronic obstructive pulmonary fixation]. Ukrainskyi pulmonolohichnyi zhurnal. 2014;3: 33-6. Ukrainian.

[14] Dorneles GP, Vianna P, Del Duca Lima D, Galant L, Dias AS, Chies JA, et al. Cytokine response to the 6-min walk test in individuals with different degrees of COPD. Clin Respir  J.  2015;10(3). Available  from:  https://onlinelibrary.wiley.com/doi/abs/10.1111/crj.12221

[15] de  Moraes  MR,  da  Costa  AC,  Corrêa  Kde  S, Junqueira-Kipnis  AP,  Rabahi  MF.  Interleukin-6  and interleukin-8 blood levels’ poor association with the severity and clinical profile of ex-smokers with COPD. Int J Chron Obstruct Pulmon Dis. 2014;9: 735-43. DOI: 10.2147/COPD.S64135

[16] Hood BI. [Express method for detecting antitrypsin and  antihemo-trypsin  in  the  blood].  Laboratornoye  delo. 1981;4: 27-9. Russian.

[17] Guidelines for management of incidental pulmonary nodules  detected  on  CT  images: From  the  Fleischner Society. Radiology. 2017. DOI10.1148/radiol.2017161659.

[18] Coxson HO, Rogers RM, Whittall KP, D'yachkova Y, Paré  PD,  Sciurba  FC,  et  al. A quantification  of  the  lung surface area in emphysema using computed tomography. Am J Respir Crit Care Med. 1999;159(3): 851-6.

[19] Pertseva ТА. Mykhailychenko DS. Relation between clinical and anthropometric data and systemic inflammation in patients with COPD. Medychni perspektyvy. 2015;4; 16-22. DOI: https://doi.org/10.26641/2307-0404.2015.4.56128