Th17/Treg Imbalance in Chronic Obstructive Pulmonary Disease: Clinical and Experimental Evidence.

The imbalance between pro- and anti-inflammatory immune responses mediated by Th17 and Treg cells is deeply involved in the development and progression of inflammation in chronic obstructive pulmonary disease (COPD). Several clinical and experimental studies have described the Th17/Treg imbalance in COPD progression. Due to its importance, many studies have also evaluated the effect of different treatments targeting Th17/Treg cells.

Chronic exposure to diesel particles worsened emphysema and increased M2-like phenotype macrophages in a PPE-induced model.

Chronic exposure to ambient levels of air pollution induces respiratory illness exacerbation by increasing inflammatory responses and apoptotic cells in pulmonary tissues. The ineffective phagocytosis of these apoptotic cells (efferocytosis) by macrophages has been considered an important factor in these pathological mechanisms. Depending on microenvironmental stimuli, macrophages can assume different phenotypes with different functional actions.

Microenvironmental stimuli induce different macrophage polarizations in experimental models of emphysema.

Macrophages play a pivotal role in the development of emphysema and depending on the microenvironment stimuli can be polarized into M1- or M2-like macrophage phenotypes. We compared macrophage polarizations in cigarette smoke (CS)- and porcine pancreatic elastase (PPE)-induced emphysema models. C57BL/6 mice were subdivided into four experimental groups.

Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model.

Background: The imbalance between pro- and anti-inflammatory immune responses plays a pivotal role in chronic obstructive pulmonary disease (COPD) development and progression. To clarify the pathophysiological mechanisms of this disease, we performed a temporal analysis of immune response-mediated inflammatory progression in a cigarette smoke (CS)-induced mouse model with a focus on the balance between Th17 and Treg responses.

Methods: C57BL/6 mice were exposed to CS for 1, 3 or 6 months to induce COPD, and the control groups were maintained under filtered air conditions for the same time intervals.

A murine model of elastase- and cigarette smoke-induced emphysema.

Objective:: To describe a murine model of emphysema induced by a combination of exposure to cigarette smoke (CS) and instillation of porcine pancreatic elastase (PPE).

Methods:: A total of 38 C57BL/6 mice were randomly divided into four groups: control (one intranasal instillation of 0.9% saline solution); PPE (two intranasal instillations of PPE); CS (CS exposure for 60 days); and CS + PPE (two intranasal instillations of PPE + CS exposure for 60 days).

Influence of Smoking Consumption and Nicotine Dependence Degree in Cardiac Autonomic Modulation.

Background: Smoking consumption alters cardiac autonomic function.

Objective: Assess the influence of the intensity of smoking and the nicotine dependence degree in cardiac autonomic modulation evaluated through index of heart rate variability (HRV).

Methods: 83 smokers, of both genders, between 50 and 70 years of age and with normal lung function were divided according to the intensity of smoking consumption (moderate and severe) and the nicotine dependency degree (mild, moderate and severe).

Nasal and systemic inflammatory profile after short term smoking cessation.

Introduction: Smoking cessation promotes health benefits and, despite cigarette smoking be an important pro inflammatory stimulus, there are few studies concerning the nasal and systemic inflammation; as well as the mucociliary clearance behavior in smokers after short period of smoking cessation.

Aim: To evaluate the nasal and systemic inflammatory markers and mucociliary clearance behavior after 30 days of cigarette smoking abstinence.

Methods: Twenty-five smokers were included and divided into two groups: abstinent smokers (n = 14) and current smokers (n = 11).

Effects of cigarette smoking intensity on the mucociliary clearance of active smokers.

Background: Smoking impairs mucociliary clearance and increases respiratory infection frequency and severity in subjects with and without smoking-related chronic lung diseases.

Objective: This study evaluated the effects of smoking intensity on mucociliary clearance in active smokers.

Methods: Seventy-five active smokers were grouped into light (1-10 cigarettes/day; n = 14), moderate (11-20 cigarettes/day; n = 34) and heavy smokers (≥21 cigarettes/day; n = 27) before starting a smoking cessation programme.