Airway Inflammation Induced by Oxidative Stress, 2nd Edition

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (10 December 2023) | Viewed by 1865

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Instituto de Ciências Biomedicas, Universidade Federal do Rio Janeiro, Rio de Janeiro 21941-590, RJ, Brazil
Interests: redox biology and inflammation related to acute and chronic lung diseases
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Special Issue Information

Dear Colleagues,

In the first volume of the Special Issue “Airway Inflammation Induced by Oxidative Stress”, we collected five original manuscripts on different themes such as hyperoxia, cigarette smoke, air pollution, and asthma, and two review manuscripts covering COPD and acute lung injuries related to oxidative stress.

Based on recent reports about COVID-19, we have noticed overwhelming evidence that oxidative stress and oxidative damage play a pivotal role in the pathogenesis of airways. In fact, the prevalence of lung diseases increased in recent years (2023 GOLD REPORT). Thus, we have decided that a second volume on the same topic would be worthwhile.

We know that sources of increased oxidative stress of airways derive from the increased burden of oxidants from environmental exposure and from the increased amounts of reactive oxygen species (ROS) and reactive nitrogen species (RNS) released from leukocytes and other cells involved in the inflammatory process in the lungs. These ROS and RNS can cause oxidative damage to DNA, lipids, carbohydrates and proteins, and in that way, mediate an array of downstream processes that contribute to the development and progression of airway diseases. They also activate resident cells in the lungs to generate chemotactic molecules that recruit additional inflammatory cells, which in turn, perpetuates oxidative stress in the airways. Collectively, these events lead to a vicious cycle of persistent inflammation, accompanied by chronic oxidative stress, which leads to disturbances in the protease–antiprotease balance, defects in tissue repair mechanisms, and accelerated apoptosis, which have all been linked to the severity and progression of different airway diseases.

Although antioxidant sources could play a useful role in the therapy of airway diseases, their clinical impact is still relatively modest at present. This Special Issue of Antioxidants, “Airway Inflammation Induced by Oxidative Stress, Volume 2”, aims to publish manuscripts that will explore all aspects of airway inflammation induced by oxidative stress by focusing on the treatment mechanism from several stimuli in airway diseases. Original papers describing recent discoveries in the field of lung redox biology and inflammation are welcome, as well as reviews from experts in this field.

Dr. Samuel Santos Valença
Guest Editor

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Published Papers (1 paper)

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14 pages, 2138 KiB  
Article
Modulation of Alveolar Macrophage Activity by Eugenol Attenuates Cigarette-Smoke-Induced Acute Lung Injury in Mice
by Maria Clara Barbosa-de-Oliveira, Paolo Oliveira-Melo, Marcos Henrique Gonçalves da Silva, Flávio Santos da Silva, Felipe Andrade Carvalho da Silva, Bruno Vinicios Silva de Araujo, Moacir Franco de Oliveira, Aristides Tadeu Correia, Sidnei Miyoshi Sakamoto, Samuel Santos Valença, Manuella Lanzetti, Martina Schmidt and Emanuel Kennedy-Feitosa
Antioxidants 2023, 12(6), 1258; https://doi.org/10.3390/antiox12061258 - 11 Jun 2023
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Abstract
This study investigates the role of eugenol (EUG) on CS-induced acute lung injury (ALI) and how this compound is able to modulate macrophage activity. C57BL/6 mice were exposed to 12 cigarettes/day/5days and treated 15 min/day/5days with EUG. Rat alveolar macrophages (RAMs) were exposed [...] Read more.
This study investigates the role of eugenol (EUG) on CS-induced acute lung injury (ALI) and how this compound is able to modulate macrophage activity. C57BL/6 mice were exposed to 12 cigarettes/day/5days and treated 15 min/day/5days with EUG. Rat alveolar macrophages (RAMs) were exposed to CSE (5%) and treated with EUG. In vivo, EUG reduced morphological changes inflammatory cells, oxidative stress markers, while, in vitro, it induced balance in the oxidative stress and reduced the pro-inflammatory cytokine release while increasing the anti-inflammatory one. These results suggest that eugenol reduced CS-induced ALI and acted as a modulator of macrophage activity. Full article
(This article belongs to the Special Issue Airway Inflammation Induced by Oxidative Stress, 2nd Edition)
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