Júlia B. Kohler
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Júlia B. Kohler has a total of 14 co-authors. Here are the top co-authors by number of shared publications:
- Alyne Riani Moreira
Laboratory of Experimental Therapeutics (LIM-20), Department of Medicine, School of Medicine, University of São Paulo, São Paulo 01246-903, Brazil
1 shared publication - Ana Paula Pereira Velosa
Rheumatology Division of the Hospital das Clinicas, University of São Paulo Medical School, São Paulo 01246 000, Brazil
1 shared publication - Denise Frediani Barbeiro
Departamento de Emergência (LIM 51), Faculdade de Medicina FMUSP, Universidade de São Paulo, Sao Paulo 01246-903, SP, Brazil
1 shared publication - Elnara Marcia Negri
Departamento de Patologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil
1 shared publication - Fernanda Degobbi Tenorio Quirino Santos Lopes
Laboratory of Experimental Therapeutics (LIM20), Department of Clinical Medicine, School of Medicine, University of Sao Paulo
1 shared publication - Frederico Leon Arrabal Fernandes
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
1 shared publication
Latest Publications
- Open Access
Th17/Treg-Related Intracellular Signaling in Patients with Chronic Obstructive Pulmonary Disease: Comparison between Local and Systemic Responses
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.
Open AccessTh17/Treg-Related Intracellular Signaling in Patients with Chronic Obstructive Pulmonary Disease: Comparison between Local and Systemic Responses
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.