Death Mechanisms of Pulmonary Alveolocytes in Mice Infected with Influenza Viruses A/H1N1/California/04/2009 and A/H5N1/Goose/Krasnoozerskoye/627/05


Дәйексөз келтіру

Толық мәтін

Ашық рұқсат Ашық рұқсат
Рұқсат жабық Рұқсат берілді
Рұқсат жабық Тек жазылушылар үшін

Аннотация

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.

Авторлар туралы

T. Sharkova

Optimum Medical Laboratory, Research-and-Educational Center

Email: cherdanceff@yandex.ru
Ресей, Sochi

V. Shkurupy

Research Institute of Experimental and Clinical Medicine, Federal Research Center of Fundamental and Translational Medicine; Novosibirsk State Medical University

Email: cherdanceff@yandex.ru
Ресей, Novosibirsk; Novosibirsk

A. Shestopalov

Research Institute of Experimental and Clinical Medicine, Federal Research Center of Fundamental and Translational Medicine

Email: cherdanceff@yandex.ru
Ресей, Novosibirsk

O. Potapova

Optimum Medical Laboratory, Research-and-Educational Center

Email: cherdanceff@yandex.ru
Ресей, Sochi

L. Cherdantseva

Research Institute of Experimental and Clinical Medicine, Federal Research Center of Fundamental and Translational Medicine

Хат алмасуға жауапты Автор.
Email: cherdanceff@yandex.ru
Ресей, Novosibirsk

A. Kovner

Research Institute of Experimental and Clinical Medicine, Federal Research Center of Fundamental and Translational Medicine

Email: cherdanceff@yandex.ru
Ресей, Novosibirsk


© Springer Science+Business Media, LLC, part of Springer Nature, 2019

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