[Retracted] N‐Acetylcysteine Improves Inflammatory Response in COPD Patients by Regulating Th17/Treg Balance through Hypoxia Inducible Factor‐1α Pathway

Abstract

Introduction. This study was aimed to investigate the effects of N-acetylcysteine (NAC) on chronic obstructive pulmonary disease (COPD) and the change of Th17/Treg cytokine imbalance. Material and Methods. A total of 121 patients with stable COPD at the stage of C or D were consecutively enrolled and randomly divided into 2 groups. Patients in the treatment group received NAC granules ( 0.2 g × 10 bags , 0.4 g each time, 3 times/d) for half a year. The control group was treated with the same amount of placebo therapy. The peripheral blood of the patient was collected and the cytokine, T lymphocyte subsets were detected. Results. We found the oral administration of NAC could regulate Th17/Treg balance to resist inflammation in COPD patients. Serum testing showed that the proportion of Treg in CD4+ T cells has increased and the Th17/Treg ratio has decreased during the NAC treatment. In vitro studies, we found that NAC regulated Th17/Treg balance through Hypoxia Inducible Factor-1α pathway. Conclusions. Our result could provide new diagnosis and treatment for elderly patients with COPD from the perspective of immunity ideas.

Mechanisms of Vitamin C Regulating Immune and Inflammation Associated with Neonatal Hypoxic-Ischemic Encephalopathy Based on Network Pharmacology and Molecular Simulation Technology

“…Many studies have confirmed that HIF1A is closely related to inflammation and the immune system. When immune cells are in a hypoxic state, activated HIF1A can regulate the survival and differentiation of immune cells such as Th17 cells through Th17 cell differentiation and other signal pathways, which has played an important role in controlling the expression of proinflammatory factors [ 57 , 58 ]. In addition, the activation of HIF1A can induce stanniocalcin-1 in astrocytes to regulate glycolysis and reduce reactive oxygen species (ROS) levels to protect cells from hypoxia in an AMPK α 1-dependent manner [ 59 ].…”

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

“…In addition, the authors demonstrated that NAC regulated Th17/Treg balance through Hypoxia Inducible Factor-1a (HIF-1a) pathway, which is molecule that can upregulate the IL-17 expression through RORgt and in addition to degrade Foxp3 (74,75). The COPD NAC-treated group showed significantly decreased HIF1-a expression of Th17 and Treg cells isolated from peripheral blood (74).…”

“…Treatment with N-Acetylcysteine (NAC), an antioxidant that works as a mucolytic agent, was also effective on restore the Th17/Treg imbalance in COPD patients ( 74 ). In this study, the oral administration of NAC for 6 months led to a decrease in Th17 cells and increase in Treg cells of PBMC from COPD treated patients compared to the nontreated group.…”

“…In this study, the oral administration of NAC for 6 months led to a decrease in Th17 cells and increase in Treg cells of PBMC from COPD treated patients compared to the nontreated group. These findings were accompanied with decreased serum levels of inflammatory cytokines such as IL-17 and IL-1β and increased of the anti-inflammatory IL-10 level ( 74 ). In addition, the authors demonstrated that NAC regulated Th17/Treg balance through Hypoxia Inducible Factor-1α (HIF-1α) pathway, which is molecule that can upregulate the IL-17 expression through RORγt and in addition to degrade Foxp3 ( 74 , 75 ).…”

“…These findings were accompanied with decreased serum levels of inflammatory cytokines such as IL-17 and IL-1β and increased of the anti-inflammatory IL-10 level ( 74 ). In addition, the authors demonstrated that NAC regulated Th17/Treg balance through Hypoxia Inducible Factor-1α (HIF-1α) pathway, which is molecule that can upregulate the IL-17 expression through RORγt and in addition to degrade Foxp3 ( 74 , 75 ). The COPD NAC-treated group showed significantly decreased HIF1-α expression of Th17 and Treg cells isolated from peripheral blood ( 74 ).…”