Death Mechanisms of Pulmonary Alveolocytes in Mice Infected with Influenza Viruses A/H1N1/California/04/2009 and A/H5N1/Goose/Krasnoozerskoye/627/05
Autor: | L. A. Cherdantseva, A. V. Kovner, V. A. Shkurupy, T. V. Sharkova, O. V. Potapova, Alexander Shestopalov |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Necrosis Apoptosis medicine.disease_cause General Biochemistry Genetics and Molecular Biology 03 medical and health sciences Mice 0302 clinical medicine Goose Influenza A Virus H1N1 Subtype Orthomyxoviridae Infections Cell surface receptor biology.animal medicine Animals FADD Lung biology Influenza A Virus H5N1 Subtype Caspase 3 virus diseases General Medicine Virology Influenza A virus subtype H5N1 Caspase 9 Pulmonary Alveoli 030104 developmental biology biology.protein Mice Inbred CBA Immunohistochemistry Signal transduction medicine.symptom 030217 neurology & neurosurgery |
Zdroj: | Bulletin of experimental biology and medicine. 166(5) |
ISSN: | 1573-8221 |
Popis: | In CBA mice infected with influenza viruses A/H1N1/California/04/2009 and A/H5N1/Goose/Krasnoozerskoye/627/05 in a dose of 10 MLD50, the mechanisms of death of pulmonary alveolocytes over 10 postinfection days were studied by light microscopy, immunohistochemistry, and morphometry. In mice infected with A/H1N1, alveolocytes died predominantly via necrosis, while apoptosis mostly employed the mitochondrial pathway. In mice infected with A/H5N1, apoptosis was the dominant mechanism of alveolocyte death proceeded via membrane receptor signaling followed by switching to FAS-mediated pathway via activation of FADD, the apoptotic signal transduction protein. |
Databáze: | OpenAIRE |
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