Morphofunctional Changes in the Lung Vascular Endotheliocytes in Mice with influenza A/H5N1 A/Goose/Krasnoozerskoye/627/05

Bull Exp Biol Med. 2013 Feb;154(4):476-479.

Kovner AV, Potapova OV, Shkurupy VA.

Research Center of Clinical and Experimental Medicine, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk, Russia.

potapova@soramn.ru

Abstract: The lung vessels of male C57Bl/6 mice were studied by immunohistochemical and stereometric methods on days 1, 3, 6, and 10 after intranasal infection with influenza A/H5N1 A/Goose/Krasnoozerskoye/627/05 virus. Influenza virus replicates in mouse lung vascular endotheliocytes and persists in these cells until the beginning of convalescence (day 10 after infection). This indicates high pathogenic activity of this strain. Active proliferation and apoptosis of endotheliocytes are detected early after infection; the counts of endotheliocytes expressing lysosomal hydrolases and NO-synthases increase many-fold.

PMID: 23486585

 

Supplementary:

High pneumotropic virus and early viremia are caused by replication of virus A/H5N1 and its persistence in pulmonary endothelial cells. Endothelial cells are involved in early antiviral response through implementation an oxygen-independent (lysozyme, сatepsin D) and oxygen-dependent (NO-synthase and myeloperoxidase) mechanisms. However, in spite of the high relevance of the study of the pathogenesis of influenza, there is a fairly complete understanding of the role “of endothelial component” in the pathogenesis of this disease in mammals.

So, infection of endothelial cells by the virus of influenza A/H5N1, appears to be a factor inducing their proliferation in the 1st study day, and activation of apoptosis in them. This accompanied by severe agitation of oxygen- and oxygen independent mechanisms of anti-viral defense by increasing the number of cells expressing lysosomal hydrolase and NO-synthase. However, this phenomenon can be sort risk factor for destructive processes light due to the high destructive potential of lysosomal hydrolases concentrated in pulmonary vascular endothelial cells, as well as risk of hypoxia due to damage of blood vessels and a high probability of thrombosis.

Oksana V. Potapov-1Fig. 1. Result for numerical density of endothelial cells expressing influenza A virus antigen in mice lungs infected with A/goose/Krasnoozerskoye/627/05 (H5N1) influenza virus.

 

Oksana V. Potapov-2

Fig. 2. Lung fragment of mice infected with A/goose/Krasnoozerskoye/627/05 (H5N1) influenza virus. Influenza A virus antigen expression by endothelial cells of mice infected with A/goose/Krasnoozerskoye/627/05 (H5N1) influenza virus. First day of experiment. Immunofluorescent analysis. Magnitude х 630.

 

Oksana V. Potapov-3Fig. 3. Estimation result for numerical density of endothelial cells expressing influenza A virus antigen and eNOS in mice lungs infected with A/goose/Krasnoozerskoye/627/05 (H5N1) influenza virus.

 

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Fig. 4. Lung fragment of mice infected with A/goose/Krasnoozerskoye/627/05 (H5N1) influenza virus. Caspase-3 expression by endothelial cells of mice infected with A/goose/Krasnoozerskoye/627/05 (H5N1) influenza virus. Sixth day of experiment. Immunohistochemical analysis. Magnitude х 400.

 

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Fig. 5. Lung fragment of mice infected with A/goose/Krasnoozerskoye/627/05 (H5N1) influenza virus. iNOS expression by endothelial cells of mice infected with A/goose/Krasnoozerskoye/627/05 (H5N1) influenza virus. Sixth day of experiment. Immunohistochemical analysis. Magnitude х400.

 

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