MARCH-APRIL 2011 | Jochen Grommes and Oliver Soehnlein
This review discusses the role of neutrophils in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). ALI and ARDS are characterized by increased permeability of the alveolar-capillary barrier, leading to lung edema and impaired arterial oxygenation. Neutrophils, the first immune cells to be recruited to the site of inflammation, play a crucial role in the progression of ALI and ARDS. The review highlights the mechanisms of neutrophil recruitment into the lung, including the involvement of selectins, integrins, chemokines, and cytokines. It also examines the contribution of neutrophil-derived granule proteins, such as serine proteases, matrix metalloproteinases (MMPs), and cationic polypeptides, to tissue damage in ALI. Additionally, the role of reactive oxygen species (ROS) and nitrogen species (RNS) produced by neutrophils in lung injury is discussed. The review concludes by emphasizing the need for therapeutic approaches to control neutrophil activity to reduce host tissue damage in ALI.This review discusses the role of neutrophils in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). ALI and ARDS are characterized by increased permeability of the alveolar-capillary barrier, leading to lung edema and impaired arterial oxygenation. Neutrophils, the first immune cells to be recruited to the site of inflammation, play a crucial role in the progression of ALI and ARDS. The review highlights the mechanisms of neutrophil recruitment into the lung, including the involvement of selectins, integrins, chemokines, and cytokines. It also examines the contribution of neutrophil-derived granule proteins, such as serine proteases, matrix metalloproteinases (MMPs), and cationic polypeptides, to tissue damage in ALI. Additionally, the role of reactive oxygen species (ROS) and nitrogen species (RNS) produced by neutrophils in lung injury is discussed. The review concludes by emphasizing the need for therapeutic approaches to control neutrophil activity to reduce host tissue damage in ALI.