Endothelial–platelet interactions in influenza‐induced pneumonia: A potential therapeutic target

Abstract

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.

Factors associated with death outcome in patients with severe coronavirus disease-19 (COVID-19): a case-control study

“…Two previous studies in the same center found significantly elevated levels of multiple serum cytokines in severe COVID-19 patients, such as IL-1β, IL-2, IL-6, TNF-α, and INF-γ, which were associated with the disease severity [3,7]. It was suspected a phenomenon named "cytokine storm" might result in the progression of the disease in viral pneumonia [28,29]. In previous studies, COVID-19 was thought to induce "cytokine storm" that then caused multi-organ impairment involving the heart, liver, and kidney [6,7,10,13].…”

Endothelial Injury and Glycocalyx Degradation in Critically Ill Coronavirus Disease 2019 Patients: Implications for Microvascular Platelet Aggregation

“…Previous studies have demonstrated that pulmonary viral infections can drive platelet–endothelial interaction through the up-regulation of endothelial intracellular adhesion molecule 1, vWF, and fibronectin leading to ongoing lung injury ( 48 ). In addition, aggregation of activated platelets within the pulmonary microvasculature not only promotes lung inflammation and injury but also propagates viral pathogenesis ( 49 ). As such, platelet interaction with activated pulmonary endothelial cells, at least in part due to glycocalyx degradation and the subsequent decrease in nitric oxide production, promotes vascular occlusion, enhances inflammation, and drives viral pathogenesis.…”

Role of Prealbumin in Predicting the Prognosis of Severely and Critically Ill COVID-19 Patients

“…A previous study involving 80 critically ill patients in the ICU also found that PAB was not suitable as the sole nutrition indicator when evaluating the nutritional status of critically ill patients. 23 The "cytokine storm" phenomenon, which is related to viral pneumonia, has been suggested to occur with COVID-19, 6,40,41 thereby increasing the severity of disease. Regarding SARS, the viral load did not lead to worsening symptoms; however, an overexuberant inflammatory response was common.…”

“…The “cytokine storm” phenomenon, which is related to viral pneumonia, has been suggested to occur with COVID-19, 6 , 40 , 41 thereby increasing the severity of disease. Regarding SARS, the viral load did not lead to worsening symptoms; however, an overexuberant inflammatory response was common.…”