TY  - JOUR
A1  - Rommel, Marcel G. E.
A1  - Milde, Christian
A1  - Eberle, Regina
A1  - Schulze, Harald
A1  - Modlich, Ute
T1  - Endothelial–platelet interactions in influenza‐induced pneumonia: A potential therapeutic target
JF  - Anatomia, Histologia, Embryologia
N2  - 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.
KW  - endothelial cell
KW  - influenza
KW  - interaction
KW  - laboratory animals
KW  - lung injury
KW  - platelet
KW  - pneumonia
KW  - therapy
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-213610
VL  - 49
IS  - 5
SP  - 606
EP  - 619
ER  - 
TY  - JOUR
A1  - Manukjan, Georgi
A1  - Wiegering, Verena
A1  - Reindl, Tobias
A1  - Strauß, Gabriele
A1  - Klopocki, Eva
A1  - Schulze, Harald
A1  - Andres, Oliver
T1  - Novel variants in FERMT3 and RASGRP2 - Genetic linkage in Glanzmann-like bleeding disorders
JF  - Pediatric Blood & Cancer
N2  - Defects of platelet intracellular signaling can result in severe platelet dysfunction. Several mutations in each of the linked genes FERMT3 and RASGRP2 on chromosome 11 causing a Glanzmann‐like bleeding phenotype have been identified so far. We report on novel variants in two unrelated pediatric patients with severe bleeding diathesis—one with leukocyte adhesion deficiency type III due to a homozygous frameshift in FERMT3 and the other with homozygous variants in both, FERMT3 and RASGRP2 . We focus on the challenging genetic and functional variant assessment and aim to accentuate the risk of obtaining misleading results due to the phenomenon of genetic linkage.
KW  - bleding disorders other than hemophilia
KW  - hematology
KW  - hemostasis and thrombosis
KW  - platelet disorders
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-208129
VL  - 67
IS  - 2
ER  -