Serial Histopathological Examination of the Lungs of Mice Infected with Influenza A Virus PR8 Strain

Fukushi, Masaya; Ito, Tateki; Oka, Teruaki; Kitazawa, Takio; Miyoshi‐Akiyama, Tohru; Kirikae, Teruo; Yamashita, Makoto; Kudo, Kohsuke

doi:10.1371/journal.pone.0021207

Cited by 77 publications

(81 citation statements)

References 30 publications

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“…This condition eventually progresses to acute respiratory distress syndrome (ARDS)-like pathological signs characterized by congested alveolar capillaries, pulmonary edema, hyaline membrane formation, and fibrin accumulation. These results are consistent with pathological findings in which ARDS was observed in mice with influenza A virus infection (17)(18)(19). In a previous study (8), both adult and aged mice showed a rapid decline in the body weight until 10 dpi.…”

Section: Discussionsupporting

confidence: 91%

Pathological Examination of Lung Tissues in Influenza A Virus-Infected Mice

et al. 2012

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SUMMARY:This study examined pathological changes in the lung tissues of young and aged mice infected with influenza virus. Young mice inoculated with influenza virus showed body weight loss at 4 days post-infection (dpi), meanwhile body weight decrease started from 9 dpi in the aged mice. We histopathologically examined the lungs of these mice. Immunohistochemical examination revealed that viral antigen-positive bronchiolar and alveolar epithelial cell numbers at 3 dpi were significantly higher in young mice than in the aged ones. Further, viral antigen-positive cells were observed at 9 dpi in the aged mice, but not in the young ones. Diffuse and severe bronchointerstitial pneumonia characterized by the accumulation of polymorphonuclear leukocytes (PMNs) was observed in young mice at 6 dpi. Histopathological changes in the aged mice were milder than those in the young mice. Moreover, T cell and macrophage accumulation in the lungs was significantly higher in the young mice than in the aged mice at 9 dpi. These results suggest that there may be a correlation between the relatively low level of infiltration of PMNs, macrophages, and T lymphocytes and the delayed body weight loss and longer lasting infections observed in the lungs of the aged mice. These findings provide detailed insights into the age-specific course of infection in young and aged populations with associated differences in lung pathology.

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Section: Discussionsupporting

confidence: 91%

Pathological Examination of Lung Tissues in Influenza A Virus-Infected Mice

et al. 2012

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“…HAP is mostly caused by opportunistic pathogens such as Pseudomonas aeruginosa, methicillin-resistant Staphylococcus aureus (MRSA), Acinetobacter baumannii and Enterobacteriaceae that tend to colonize patients very quickly once admitted to the hospital (13,14). In particular, infections caused by Gram-negative multidrugresistant organisms, including P. aeruginosa and extendedspectrum β-lactamase-producing or carbapenemaseproducing Enterobacteriaceae, are increasingly being reported worldwide (15).…”

Section: Etiology Of Hospital Acquired Pneumoniamentioning

confidence: 99%

Animal models of hospital-acquired pneumonia: current practices and future perspectives

Bielen¹,

Jongers²,

Malhotra-Kumar³

et al. 2017

Ann. Transl. Med.

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Lower respiratory tract infections are amongst the leading causes of mortality and morbidity worldwide. Especially in hospital settings and more particularly in critically ill ventilated patients, nosocomial pneumonia is one of the most serious infectious complications frequently caused by opportunistic pathogens.Pseudomonas aeruginosa is one of the most important causes of ventilator-associated pneumonia as well as the major cause of chronic pneumonia in cystic fibrosis patients. Animal models of pneumonia allow us to investigate distinct types of pneumonia at various disease stages, studies that are not possible in patients.Different animal models of pneumonia such as one-hit acute pneumonia models, ventilator-associated pneumonia models and biofilm pneumonia models associated with cystic fibrosis have been extensively studied and have considerably aided our understanding of disease pathogenesis and testing and developing new treatment strategies. The present review aims to guide investigators in choosing appropriate animal pneumonia models by describing and comparing the relevant characteristics of each model using P. aeruginosa as a model etiology for hospital-acquired pneumonia. Key to establishing and studying these animal models of infection are well-defined end-points that allow precise monitoring and characterization of disease development that could ultimately aid in translating these findings to patient populations in order to guide therapy. In this respect, and discussed here, is the development of humanized animal models of bacterial pneumonia that could offer unique advantages to study bacterial virulence factor expression and host cytokine production for translational purposes.

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“…The only study documenting hyaline membrane formation in mice describes them in animals that have succumbed naturally several days after influenza infection rather than being euthanized at a defined time point (Fukushi et al 2011). This finding suggests that hyaline membrane formation may occur in mice under certain circumstances.…”

Section: Main Feature: Measurement Of Histological Evidence Of Tissuementioning

confidence: 99%

Mouse Models of Acute Respiratory Distress Syndrome

Aeffner¹,

2015

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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.

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Serial Histopathological Examination of the Lungs of Mice Infected with Influenza A Virus PR8 Strain

Cited by 77 publications

References 30 publications

Pathological Examination of Lung Tissues in Influenza A Virus-Infected Mice

Pathological Examination of Lung Tissues in Influenza A Virus-Infected Mice

Animal models of hospital-acquired pneumonia: current practices and future perspectives

Mouse Models of Acute Respiratory Distress Syndrome

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