Platelet Activation and Aggregation Promote Lung Inflammation and Influenza Virus Pathogenesis

[tetano]

Am J Respir Crit Care Med. 2015 Feb 9. [Epub ahead of print]
[h=1]Platelet Activation and Aggregation Promote Lung Inflammation and Influenza Virus Pathogenesis.[/h] L? VB[SUP]1[/SUP], Schneider JG, Boergeling Y, Berri F, Ducatez M, Guerin JL, Adrian I, Errazuriz-Cerda E, Frasquilho S, Antunes L, Lina B, Bordet JC, Jandrot-Perrus M, Ludwig S, Riteau B.
[h=3]Author information[/h]

[h=3]Abstract[/h] Rationale: The hallmark of severe influenza virus infections is excessive inflammation of the lungs. Platelets are activated during influenza, but their role in influenza virus pathogenesis and inflammatory responses is unknown. Objectives: To determine the role of platelets during influenza A virus (IAV) infections and propose new therapeutics against influenza. Methods: We used targeted gene deletion approaches and pharmacological interventions to investigate the role of platelets during influenza virus infection in mice. Measurements and Main Results: Lungs of infected mice were massively infiltrated by aggregates of activated platelets. Platelet activation promoted IAV pathogenesis. Activating protease-activated receptor 4 (PAR4), a platelet receptor for thrombin that is crucial for platelet activation, exacerbated influenza-induced acute lung injury and death. In contrast, deficiency in the major platelet receptor glycoprotein IIIa (GPIIIa) protected mice from death caused by influenza viruses, and treating the mice with a specific GPIIbIIIa antagonist, eptifibatide, had the same effect. Interestingly, mice treated with other anti-platelet compounds (antagonists of PAR4, MRS 2179, and clopidogrel) were also protected from severe lung injury and lethal infections induced by several influenza strains. Conclusions: The intricate relationship between hemostasis and inflammation has major consequences in influenza virus pathogenesis, and anti-platelet drugs might be explored to develop new anti-inflammatory treatment against influenza virus infections. Key words: Lung injury, novel drugs, Flu pathogenesis, pneumonia, platelets.


[h=4]KEYWORDS:[/h] Flu pathogenesis; Lung injury; Platelets; novel drugs; pneumonia

PMID: 25664391 [PubMed - as supplied by publisher]

 

[gsgs]

[ platelets = thrombocytes = Blutplaettchen = plaquettaire ]

here is a new paper that links influenza (H1N1 only ?!) with myocardial infaction
through platelets activation

http://journals.plos.org/plosone/art...l.pone.0132259
Conclusions
A viral GES[gene expression signature] of non-specific, respiratory viral infection was associated
with acute MI[myocardial infarction]; 18% of the top 49 genes in the viral GES are involved with
hemostasis and/or platelet aggregation. Separately, H1N1 exposure, but not exposure to other
respiratory viruses, increased a platelet GES previously shown to be associated with MI.
Together, these results highlight specific genes and pathways that link viral infection,
platelet activation, and MI especially in the case of H1N1 influenza infection.