Defective formyl peptide receptor 2/3 and annexin A1 expressions associated with M2a polarization of blood immune cells in patients with chronic obstructive pulmonary disease
Abstract Background Controversy exists in previous studies on macrophage M1/M2 polarization in chronic obstructive pulmonary disease (COPD). We hypothesized that formyl peptide receptor (FPR), a marker of efferocytosis and mediator of M1/M2 polarization, may be involved in the development of COPD. M...
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doaj-43729bbcc8e24b0ca9162298fc1e63162020-11-24T21:40:42ZengBMCJournal of Translational Medicine1479-58762018-03-0116111210.1186/s12967-018-1435-5Defective formyl peptide receptor 2/3 and annexin A1 expressions associated with M2a polarization of blood immune cells in patients with chronic obstructive pulmonary diseaseYung-Che Chen0Meng-Chih Lin1Chih-Hung Lee2Shih-Feng Liu3Chin-Chou Wang4Wen-Feng Fang5Tung-Ying Chao6Chao-Chien Wu7Yu-Feng Wei8Huang-Chih Chang9Chia-Cheng Tsen10Hung-Chen Chen11Taiwan Clinical Trial Consortium of Respiratory Disease (TCORE) groupDivision of Pulmonary and Critical Care Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of MedicineDivision of Pulmonary and Critical Care Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of MedicineMedical Department, College of Medicine, Chang Gung UniversityDivision of Pulmonary and Critical Care Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of MedicineDivision of Pulmonary and Critical Care Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of MedicineDivision of Pulmonary and Critical Care Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of MedicineDivision of Pulmonary and Critical Care Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of MedicineDivision of Pulmonary and Critical Care Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of MedicineDepartment of Internal Medicine, E-Da Hospital, I-Shou UniversityDivision of Pulmonary and Critical Care Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of MedicineDivision of Pulmonary and Critical Care Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of MedicineDivision of Pulmonary and Critical Care Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of MedicineAbstract Background Controversy exists in previous studies on macrophage M1/M2 polarization in chronic obstructive pulmonary disease (COPD). We hypothesized that formyl peptide receptor (FPR), a marker of efferocytosis and mediator of M1/M2 polarization, may be involved in the development of COPD. Methods We examined FPR 1/2/3 expressions of blood M1/M2a monocyte, neutrophil, natural killer (NK) cell, NK T cell, T helper (Th) cell, and T cytotoxic (Tc) cell by flowcytometry method in 40 patients with cigarette smoking-related COPD and 16 healthy non-smokers. Serum levels of five FPR ligands were measured by ELISA method. Results The COPD patients had lower M2a percentage and higher percentages of NK, NK T, Th, and Tc cells than the healthy non-smokers. FPR2 expressions on Th/Tc cells, FPR3 expressions of M1, M2a, NK, NK T, Th, and Tc cells, and serum annexin A1 (an endogenous FPR2 ligand) levels were all decreased in the COPD patients as compared with that in the healthy non-smokers. FPR1 expression on neutrophil was increased in the COPD patient with a high MMRC dyspnea scale, while FPR2 expression on neutrophil and annexin A1 were both decreased in the COPD patients with a history of frequent moderate exacerbation (≥ 2 events in the past 1 year). In 10 COPD patients whose blood samples were collected again after 1-year treatment, M2a percentage, FPR3 expressions of M1/NK/Th cells, FPR2 expression on Th cell, and FPR1 expression on neutrophil were all reversed to normal, in parallel with partial improvement in small airway dysfunction. Conclusions Our findings provide evidence for defective FPR2/3 and annexin A1 expressions that, associated with decreased M2a polarization, might be involved in the development of cigarette smoking induced persistent airflow limitation in COPD.http://link.springer.com/article/10.1186/s12967-018-1435-5Formyl peptide receptor 1/2/3M2a polarizationChronic obstructive pulmonary diseaseCigarette smokingAnnexin A1 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Yung-Che Chen Meng-Chih Lin Chih-Hung Lee Shih-Feng Liu Chin-Chou Wang Wen-Feng Fang Tung-Ying Chao Chao-Chien Wu Yu-Feng Wei Huang-Chih Chang Chia-Cheng Tsen Hung-Chen Chen Taiwan Clinical Trial Consortium of Respiratory Disease (TCORE) group |
spellingShingle |
Yung-Che Chen Meng-Chih Lin Chih-Hung Lee Shih-Feng Liu Chin-Chou Wang Wen-Feng Fang Tung-Ying Chao Chao-Chien Wu Yu-Feng Wei Huang-Chih Chang Chia-Cheng Tsen Hung-Chen Chen Taiwan Clinical Trial Consortium of Respiratory Disease (TCORE) group Defective formyl peptide receptor 2/3 and annexin A1 expressions associated with M2a polarization of blood immune cells in patients with chronic obstructive pulmonary disease Journal of Translational Medicine Formyl peptide receptor 1/2/3 M2a polarization Chronic obstructive pulmonary disease Cigarette smoking Annexin A1 |
author_facet |
Yung-Che Chen Meng-Chih Lin Chih-Hung Lee Shih-Feng Liu Chin-Chou Wang Wen-Feng Fang Tung-Ying Chao Chao-Chien Wu Yu-Feng Wei Huang-Chih Chang Chia-Cheng Tsen Hung-Chen Chen Taiwan Clinical Trial Consortium of Respiratory Disease (TCORE) group |
author_sort |
Yung-Che Chen |
title |
Defective formyl peptide receptor 2/3 and annexin A1 expressions associated with M2a polarization of blood immune cells in patients with chronic obstructive pulmonary disease |
title_short |
Defective formyl peptide receptor 2/3 and annexin A1 expressions associated with M2a polarization of blood immune cells in patients with chronic obstructive pulmonary disease |
title_full |
Defective formyl peptide receptor 2/3 and annexin A1 expressions associated with M2a polarization of blood immune cells in patients with chronic obstructive pulmonary disease |
title_fullStr |
Defective formyl peptide receptor 2/3 and annexin A1 expressions associated with M2a polarization of blood immune cells in patients with chronic obstructive pulmonary disease |
title_full_unstemmed |
Defective formyl peptide receptor 2/3 and annexin A1 expressions associated with M2a polarization of blood immune cells in patients with chronic obstructive pulmonary disease |
title_sort |
defective formyl peptide receptor 2/3 and annexin a1 expressions associated with m2a polarization of blood immune cells in patients with chronic obstructive pulmonary disease |
publisher |
BMC |
series |
Journal of Translational Medicine |
issn |
1479-5876 |
publishDate |
2018-03-01 |
description |
Abstract Background Controversy exists in previous studies on macrophage M1/M2 polarization in chronic obstructive pulmonary disease (COPD). We hypothesized that formyl peptide receptor (FPR), a marker of efferocytosis and mediator of M1/M2 polarization, may be involved in the development of COPD. Methods We examined FPR 1/2/3 expressions of blood M1/M2a monocyte, neutrophil, natural killer (NK) cell, NK T cell, T helper (Th) cell, and T cytotoxic (Tc) cell by flowcytometry method in 40 patients with cigarette smoking-related COPD and 16 healthy non-smokers. Serum levels of five FPR ligands were measured by ELISA method. Results The COPD patients had lower M2a percentage and higher percentages of NK, NK T, Th, and Tc cells than the healthy non-smokers. FPR2 expressions on Th/Tc cells, FPR3 expressions of M1, M2a, NK, NK T, Th, and Tc cells, and serum annexin A1 (an endogenous FPR2 ligand) levels were all decreased in the COPD patients as compared with that in the healthy non-smokers. FPR1 expression on neutrophil was increased in the COPD patient with a high MMRC dyspnea scale, while FPR2 expression on neutrophil and annexin A1 were both decreased in the COPD patients with a history of frequent moderate exacerbation (≥ 2 events in the past 1 year). In 10 COPD patients whose blood samples were collected again after 1-year treatment, M2a percentage, FPR3 expressions of M1/NK/Th cells, FPR2 expression on Th cell, and FPR1 expression on neutrophil were all reversed to normal, in parallel with partial improvement in small airway dysfunction. Conclusions Our findings provide evidence for defective FPR2/3 and annexin A1 expressions that, associated with decreased M2a polarization, might be involved in the development of cigarette smoking induced persistent airflow limitation in COPD. |
topic |
Formyl peptide receptor 1/2/3 M2a polarization Chronic obstructive pulmonary disease Cigarette smoking Annexin A1 |
url |
http://link.springer.com/article/10.1186/s12967-018-1435-5 |
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