tetano
Editor, Senior Moderator
Anat Histol Embryol. 2019 Dec 2. doi: 10.1111/ahe.12521. [Epub ahead of print] [h=1]Endothelial-platelet interactions in influenza-induced pneumonia: A potential therapeutic target.[/h]
Rommel MGE[SUP]1[/SUP], Milde C[SUP]1[/SUP], Eberle R[SUP]2[/SUP], Schulze H[SUP]3[/SUP], Modlich U[SUP]1[/SUP].
[h=3]Author information[/h] 1 Research Group for Gene Modification in Stem Cells, Division of Veterinary Medicine, Paul-Ehrlich-Institut, Langen, Germany. 2 Department of Morphology, Division of Immunology, Paul-Ehrlich-Institut, Langen, Germany. 3 Institute of Experimental Biomedicine, University Hospital W?rzburg, W?rzburg, Germany.
[h=3]Abstract[/h] Every year, influenza viruses spread around the world, infecting the respiratory systems of countless humans and animals, causing illness and even death. Severe influenza infection is associated with pulmonary epithelial damage and endothelial dysfunction leading to acute lung injury (ALI). There is evidence that an aggressive cytokine storm and cell damage in lung capillaries as well as endothelial/platelet interactions contribute to vascular leakage, pro-thrombotic milieu and infiltration of immune effector cells. To date, treatments for ALI caused by influenza are limited to antiviral drugs, active ventilation or further symptomatic treatments. In this review, we summarize the mechanisms of influenza-mediated pathogenesis, permissive animal models and histopathological changes of lung tissue in both mice and men and compare it with histological and electron microscopic data from our own group. We highlight the molecular and cellular interactions between pulmonary endothelium and platelets in homeostasis and influenza-induced pathogenesis. Finally, we discuss novel therapeutic targets on platelets/endothelial interaction to reduce or resolve ALI.
? 2019 The Authors. Anatomia, Histologia, Embryologia Published by Blackwell Verlag GmbH.
[h=4]KEYWORDS:[/h] endothelial cell; influenza; interaction; laboratory animals; lung injury; platelet; pneumonia; therapy
PMID: 31793053 DOI: 10.1111/ahe.12521
Rommel MGE[SUP]1[/SUP], Milde C[SUP]1[/SUP], Eberle R[SUP]2[/SUP], Schulze H[SUP]3[/SUP], Modlich U[SUP]1[/SUP].
[h=3]Author information[/h] 1 Research Group for Gene Modification in Stem Cells, Division of Veterinary Medicine, Paul-Ehrlich-Institut, Langen, Germany. 2 Department of Morphology, Division of Immunology, Paul-Ehrlich-Institut, Langen, Germany. 3 Institute of Experimental Biomedicine, University Hospital W?rzburg, W?rzburg, Germany.
[h=3]Abstract[/h] Every year, influenza viruses spread around the world, infecting the respiratory systems of countless humans and animals, causing illness and even death. Severe influenza infection is associated with pulmonary epithelial damage and endothelial dysfunction leading to acute lung injury (ALI). There is evidence that an aggressive cytokine storm and cell damage in lung capillaries as well as endothelial/platelet interactions contribute to vascular leakage, pro-thrombotic milieu and infiltration of immune effector cells. To date, treatments for ALI caused by influenza are limited to antiviral drugs, active ventilation or further symptomatic treatments. In this review, we summarize the mechanisms of influenza-mediated pathogenesis, permissive animal models and histopathological changes of lung tissue in both mice and men and compare it with histological and electron microscopic data from our own group. We highlight the molecular and cellular interactions between pulmonary endothelium and platelets in homeostasis and influenza-induced pathogenesis. Finally, we discuss novel therapeutic targets on platelets/endothelial interaction to reduce or resolve ALI.
? 2019 The Authors. Anatomia, Histologia, Embryologia Published by Blackwell Verlag GmbH.
[h=4]KEYWORDS:[/h] endothelial cell; influenza; interaction; laboratory animals; lung injury; platelet; pneumonia; therapy
PMID: 31793053 DOI: 10.1111/ahe.12521