Genetic, transcriptomic, inflammatory and oxidative status alterations in smokers and in patients with chronic obstructive pulmonary disease

• Grant number: 15/10564-4
• Support Opportunities: Regular Research Grants
• Duration: February 01, 2017 - January 31, 2019
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal Investigator: Irma de Godoy
• Grantee: Irma de Godoy
• Host Institution: Faculdade de Medicina (FMB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil
• Associated researchers: Camila Renata Corrêa ; Mariana Gobbo Braz ; Renata Ferrari ; Suzana Erico Tanni

Abstract

Smoking is a chronic disease and the leading preventable cause of death worldwide; it is related to more than 50 diseases, including chronic obstructive pulmonary disease (COPD). COPD is defined as a preventable and treatable disease with systemic effects that can contribute to the severity of the patient. In addition to chronic inflammation, apoptosis, extracellular matrix degradation and the immune response are important events in the pathogenesis of COPD. Characterization of markers of oxidative stress and inflammation in smokers and patients with mild/moderate COPD and the difference between the two groups have potential to contribute to the understanding of the pathophysiology of the disease. In research developed in the doctoral course entitled "Association between oxidative stress, inflammation and systemic manifestations in smokers and patients with mild to moderate COPD" (Protocol CEP 4415-2012), thirty-two active smokers (smoking history e 10 pack / years) without COPD and 32 active smokers (smoking history e 10 pack / years) or former smokers with mild/moderate COPD, selected consecutively among those who are followed at Ambulatory of Pneumology and Cessation of Smoking, Botucatu Medical School (UNESP) were evaluated. Thirty-two non-smokers were included in the control group of the study. The oxidative stress markers are increased and are similar in active smokers and patients with mild disease compared with controls; however, the increase of the tumor necrosis factor receptor - TNFR2 was an early marker of COPD. This study did not evaluate the different pathways of gene expression and its association with systemic inflammation and oxidative stress in the peripheral blood of smokers without obstruction and mild to moderate COPD. The hypothesis of the current study is that smokers and patients with mild/moderate COPD present specific alterations in the expression of transcripts in peripheral blood, to identify differences between smokers and patients with mild/moderate obstruction, and could be used in future as genetic markers risk and disease progression. The current proposal will analyze the biological material (peripheral venous blood) collected in the doctoral study summarized above. (AU)