| Autor: |
Lourenço JD; Laboratory of Experimental Therapeutics, Department of Clinical Medicine, School of Medicine, University of Sao Paulo, Av. Dr. Arnaldo 455-Room 1220, Sao Paulo 01246-903, Brazil., Teodoro WR; Rheumatology Division of the Hospital das Clinicas FMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Av. Dr. Arnaldo 455-Room 3124, Sao Paulo 01246-903, Brazil., Barbeiro DF; Laboratory of Clinical Emergencies, Department of Clinical Medicine, School of Medicine, University of Sao Paulo, Av. Dr. Arnaldo 455-Room 3132, Sao Paulo 01246-903, Brazil., Velosa APP; Rheumatology Division of the Hospital das Clinicas FMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Av. Dr. Arnaldo 455-Room 3124, Sao Paulo 01246-903, Brazil., Silva LEF; Laboratory of Experimental Therapeutics, Department of Clinical Medicine, School of Medicine, University of Sao Paulo, Av. Dr. Arnaldo 455-Room 1220, Sao Paulo 01246-903, Brazil., Kohler JB; Laboratory of Experimental Therapeutics, Department of Clinical Medicine, School of Medicine, University of Sao Paulo, Av. Dr. Arnaldo 455-Room 1220, Sao Paulo 01246-903, Brazil., Moreira AR; Laboratory of Experimental Therapeutics, Department of Clinical Medicine, School of Medicine, University of Sao Paulo, Av. Dr. Arnaldo 455-Room 1220, Sao Paulo 01246-903, Brazil., Aun MV; Host & Defense Unit, Faculdade Israelita de Ciências da Saúde Albert Einstein School of Medicine, Av. Prof. Francisco Morato 4.293, Sao Paulo 05521-200, Brazil.; Clinical Immunology and Allergy Division, School of Medicine, University of Sao Paulo, Av. Dr. Enéas de Carvalho Aguiar 155-8th. Floor, Sao Paulo 05403-000, Brazil., da Silva IC; Pulmonary Division-Heart Institute of Hospital das Clinicas, School of Medicine of University of Sao Paulo, Av. Dr. Enéas Carvalho Aguiar 44, Sao Paulo 05403-000, Brazil., Fernandes FLA; Pulmonary Division-Heart Institute of Hospital das Clinicas, School of Medicine of University of Sao Paulo, Av. Dr. Enéas Carvalho Aguiar 44, Sao Paulo 05403-000, Brazil., Negri EM; Laboratory of Cellular Biology, Department of Pathology, School of Medicine, University of Sao Paulo, Av. Dr. Arnaldo 455-Room 4349, Sao Paulo 01246-903, Brazil., Gross JL; Department of Thoracic Surgery, A C Camargo Cancer Center, R. Prof Antonio Prudente 211, Sao Paulo 01509-010, Brazil., Tibério IFLC; Laboratory of Experimental Therapeutics, Department of Clinical Medicine, School of Medicine, University of Sao Paulo, Av. Dr. Arnaldo 455-Room 1220, Sao Paulo 01246-903, Brazil., Ito JT; Laboratory of Experimental Therapeutics, Department of Clinical Medicine, School of Medicine, University of Sao Paulo, Av. Dr. Arnaldo 455-Room 1220, Sao Paulo 01246-903, Brazil., Lopes FDTQS; Laboratory of Experimental Therapeutics, Department of Clinical Medicine, School of Medicine, University of Sao Paulo, Av. Dr. Arnaldo 455-Room 1220, Sao Paulo 01246-903, Brazil. |
| Abstrakt: |
Th17/Treg imbalance plays a pivotal role in COPD development and progression. We aimed to assess Th17/Treg-related intracellular signaling at different COPD stages in local and systemic responses. Lung tissue and/or peripheral blood samples were collected and divided into non-obstructed (NOS), COPD stages I and II, and COPD stages III and IV groups. Gene expression of STAT3 and -5 , RORγt , Foxp3 , interleukin (IL)-6 , -17 , -10 , and TGF-β was assessed by RT-qPCR. IL-6, -17, -10, and TGF-β levels were determined by ELISA. We observed increased STAT3 , RORγt , Foxp3 , IL-6 , and TGF-β gene expression and IL-6 levels in the lungs of COPD I and II patients compared to those of NOS patients. Regarding the systemic response, we observed increased STAT3 , RORγt , IL-6 , and TGF-β gene expression in the COPD III and IV group and increased IL-6 levels in the COPD I and II group. STAT5 was increased in COPD III and IV patients, although there was a decrease in Foxp3 expression and IL-10 levels in the COPD I and II and COPD III and IV groups, respectively. We demonstrated that an increase in Th17 intracellular signaling in the lungs precedes this increase in the systemic response, whereas Treg intracellular signaling varies between the compartments analyzed in different COPD stages. |
