Mouse Models of Acute Respiratory Distress Syndrome

Abstract

Acute respiratory distress syndrome (ARDS) is a severe pulmonary reaction requiring hospitalization, which is incited by many causes, including bacterial and viral pneumonia as well as near drowning, aspiration of gastric contents, pancreatitis, intravenous drug use, and abdominal trauma. In humans, ARDS is very well defined by a list of clinical parameters. However, until recently no consensus was available regarding the criteria of ARDS that should be evident in an experimental animal model. This lack was rectified by a 2011 workshop report by the American Thoracic Society, which defined the main features proposed to delineate the presence of ARDS in laboratory animals. These should include histological changes in parenchymal tissue, altered integrity of the alveolar capillary barrier, inflammation, and abnormal pulmonary function. Murine ARDS models typically are defined by such features as pulmonary edema and leukocyte infiltration in cytological preparations of bronchoalveolar lavage fluid and/or lung sections. Common pathophysiological indicators of ARDS in mice include impaired pulmonary gas exchange and histological evidence of inflammatory infiltrates into the lung. Thus, morphological endpoints remain a vital component of data sets assembled from animal ARDS models.

Lipopolysaccharide-induced endotoxemia in corn oil-preloaded mice causes an extended course of lung injury and repair and pulmonary fibrosis: A translational mouse model of acute respiratory distress syndrome

“…pneumonia, inhalation injury, aspiration of gastric contents, pulmonary contusion, or reperfusion pulmonary edema) or indirect (e.g. sepsis, burn, major trauma with shock, multiple blood transfusions, or acute pancreatitis) [1, 2, 4]. ARDS in humans is defined by a list of clinical parameters including diffuse alveolar damage and reduced pulmonary oxygenation [1, 2, 5, 6].…”

“…Mouse models of sepsis-induced inflammatory lung injury can be used to improve understanding of the mechanisms that control sepsis-induced lung injury and subsequent repair [4, 11]. It is therefore desirable for such mouse models to recapitulate the pathogenesis of human ARDS as closely as possible.…”

Histopathologic Evaluation and Scoring of Viral Lung Infection

“…Preparation of quality lung tissue samples is important for histopathologic examination to optimize preservation of fine pulmonary architecture and, in the case of immunostaining, antigenicity of target epitopes [11][12][13]. A study by Engel and Moore identified more than 60 variables in this time frame, beginning with proper sample collection and handling and including multiple aspects of tissue collection, fixation, processing, embedding, slide drying, and storage [14].…”

“…To collect lungs for histology, samples should be harvested as soon as possible following death to minimize autolysis [11]. Autolysis ("self-digestion") is a postmortem change characterized by degradation of cellular constituents (DNA, RNA, protein) and dissolution of the tissue [15].…”

Seawater-drowning-induced acute lung injury: From molecular mechanisms to potential treatments

“…However, barrier disruption differs with injury type. Pulmonary edema causes pulmonary interstitium thickening and alters the gas exchange process by increasing the distance for gas exchange to occur (43), whereas lipopolysaccharide-induced acute lung injury predominantly damages pulmonary microvascular endothelial cells and destroys their barrier function, thereby causing inflammatory cell aggregation, adhesion, exudation and secretion of various inflammatory cytokines and chemokines (44). As a result, the blood barrier is further damaged.…”