About this Research Topic
Acute respiratory distress syndrome (ARDS), a frequently occurring and severe pulmonary complication of critical illness, affects around 12%-20% of patients who are hospitalized in the intensive care unit. Despite the advances made in clinical management and basic science, severe ARDS continues to have a high mortality rate of 35%–47%. A more comprehensive understanding of the underlying mechanisms of ARDS is necessary to develop new and effective therapies that can improve patient outcomes. Therefore, continued research efforts are essential to identify novel therapeutic targets and to develop new treatment strategies that can prevent or mitigate the damage caused by ARDS.
Uncontrolled inflammatory reactions in the lungs bring about the prolongation of lung injury which worsens the severity of ARDS and the prognosis of the patient. Macrophages/monocytes play a pivotal role in this pathogenesis. Several studies have demonstrated that macrophage polarization plays a critical role in the inflammatory process of ARDS. M1-polarized macrophages produce pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1beta), and interleukin-6 (IL-6), which contribute to the recruitment and activation of immune cells, and the damage to alveolar epithelium and endothelial cells. In contrast, M2-polarized macrophages produce anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-beta), which promote tissue repair and resolution of inflammation. The balance between M1 and M2 polarization is critical in determining the overall inflammatory response and tissue damage in ARDS. A better understanding of the molecular control of macrophage phenotypic switching in ARDS could uncover potential therapeutic targets. The aim of this Research Topic is to create a platform to promote research on the role of macrophage polarization in the initiation and progression of ARDS and to investigate novel pharmacological interventions that could have a positive impact on ARDS.
The goal of this Research Topic is to bring together experts from different fields to share their insights and collaborate on research that can lead to innovative solutions and new treatment strategies for ARDS. By focusing on the molecular mechanisms underlying macrophage polarization in ARDS pathogenesis, researchers can identify novel therapeutic targets and develop more effective treatments that can alleviate the severity of ARDS and improve patient outcomes. This interdisciplinary approach can accelerate progress in the field and ultimately lead to better outcomes for ARDS patients.
Those bullet points are appropriate for a Research Topic on "Macrophage Polarization in ARDS." They cover the key areas of interest related to:
(1) Novel molecules and mechanisms in macrophage polarization;
(2) Role of macrophage polarization on the genesis and development of ARDS;
(3) Inflammatory damage of M1-polarized macrophages on the alveolar epithelium and endothelial cells;
(4) Role of M2-polarized macrophages on the repair and pulmonary fibrosis during ARDS;
(5) The association between macrophage polarization and prognosis and severity of ARDS patients.
Uncontrolled inflammatory reactions in the lungs bring about the prolongation of lung injury which worsens the severity of ARDS and the prognosis of the patient. Macrophages/monocytes play a pivotal role in this pathogenesis. Several studies have demonstrated that macrophage polarization plays a critical role in the inflammatory process of ARDS. M1-polarized macrophages produce pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1beta), and interleukin-6 (IL-6), which contribute to the recruitment and activation of immune cells, and the damage to alveolar epithelium and endothelial cells. In contrast, M2-polarized macrophages produce anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-beta), which promote tissue repair and resolution of inflammation. The balance between M1 and M2 polarization is critical in determining the overall inflammatory response and tissue damage in ARDS. A better understanding of the molecular control of macrophage phenotypic switching in ARDS could uncover potential therapeutic targets. The aim of this Research Topic is to create a platform to promote research on the role of macrophage polarization in the initiation and progression of ARDS and to investigate novel pharmacological interventions that could have a positive impact on ARDS.
The goal of this Research Topic is to bring together experts from different fields to share their insights and collaborate on research that can lead to innovative solutions and new treatment strategies for ARDS. By focusing on the molecular mechanisms underlying macrophage polarization in ARDS pathogenesis, researchers can identify novel therapeutic targets and develop more effective treatments that can alleviate the severity of ARDS and improve patient outcomes. This interdisciplinary approach can accelerate progress in the field and ultimately lead to better outcomes for ARDS patients.
Those bullet points are appropriate for a Research Topic on "Macrophage Polarization in ARDS." They cover the key areas of interest related to:
(1) Novel molecules and mechanisms in macrophage polarization;
(2) Role of macrophage polarization on the genesis and development of ARDS;
(3) Inflammatory damage of M1-polarized macrophages on the alveolar epithelium and endothelial cells;
(4) Role of M2-polarized macrophages on the repair and pulmonary fibrosis during ARDS;
(5) The association between macrophage polarization and prognosis and severity of ARDS patients.
Keywords: Macrophage Polarization, ARDS
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