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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\u2010thrombotic 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\u2010mediated 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\u2010induced pathogenesis. Finally, we discuss novel therapeutic targets on platelets\/endothelial interaction to reduce or resolve ALI.<\/jats:p>","DOI":"10.1111\/ahe.12521","type":"journal-article","created":{"date-parts":[[2019,12,3]],"date-time":"2019-12-03T07:14:43Z","timestamp":1575357283000},"page":"606-619","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Endothelial\u2013platelet interactions in influenza\u2010induced pneumonia: A potential therapeutic target"],"prefix":"10.1111","volume":"49","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4861-3175","authenticated-orcid":false,"given":"Marcel G. 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