Vascular endothelium and infectious diseases: Trick and treat

• References

• 1 Cossart P, Boquet P, Normark S, Rappuoli R. Cellular Microbiology.. 2nd edition ASM Press; Washington D. C.: 2005
• 2 Ebihara H, Groseth A, Neumann G. et al. The role of reverse genetics systems in studying viral hemorrhagic fevers. Thromb Haemost 2005; 94: 240-53.
• 3 Hensley LE, Geisbert TW. The contribution of the endothelium to the development of coagulation disorders that characterize Ebola haemorrhagic fever in primates. Thromb Haemost 2005; 94: 254-61.
• 4 Klenk HD. Infection of the endothelium by influenza viruses. Thromb Haemost 2005; 94: 262-5.
• 5 Sinha B, Herrmann M. Mechanism and consequences of invasion of endothelial cells by Staphylococcus aureus. Thromb Haemost 2005; 94: 266-77.
• 6 Chavakis T, Wiechmann K, Preissner KT. et al. Staphylococcus aureus interactions with the endothelium: The role of bacterial ‘‘Secretable Expanded Repertoire Adhesive Molecules” (SERAM) in disturbing host defense systems. Thromb Haemost 2005; 94: 278-85.
• 7 Liu CZ, Shih MH, Tsai PJ. ClfA221–550, a fibrinogen- binding segment of Staphylococcus aureus clumping factor A, disrupts fibrinogen function. Thromb Haemost 2005; 94: 286-94.
• 8 Dje N' Guessan P, Schmeck B, Ayim A. et al. Streptococcus pneumoniae R6x induced p38 mapk and jnkmediated caspase-dependent apoptosis in human endothelial cells. Thromb Haemost 2005; 94: 295-303.
• 9 Bergmann S, Rohde M, Preissner KT. et al. The nine residue plasminogen-binding motif of the pneumococcal enolase is the major cofactor of plasmin-mediated degradation of extracellular matrix, dissolution of fibrin and transmigration. Thromb Haemost 2005; 94: 304-11.
• 10 Bielaszewska M, Karch H. Consequences of enterohaemorrhagic escherichia coli infection for the vascular endothelium. Thromb Haemost 2005; 94: 312-8.
• 11 Krüll M, Maass M, Suttorp N. et al. Chlamydophila pneumoniae – mechanisms of target cell infection and activation. Thromb Haemost 2005; 94: 319-26.
• 12 Kälvegren H, Bylin H, Leanderson P. et al. Chlamydia pneumoniae induces nitric oxide synthase and lipoxygenase- dependent production of reactive oxygen species in platelets – effects on oxidation of low density lipoproteins. Thromb Haemost 2005; 94: 327-35.
• 13 Pino P, Taoufiq Z, Nitcheu J. et al. Blood-brain barrier breakdown during cerebral malaria: Suicide or murder?. Thromb Haemost 2005; 94: 336-40.
• 14 Adam RA, Rüssing D, Adams O. et al. Role of human brain microvascular endothelial cells during CNS infection: significance of indoleamine 2,3-dioxygenase in antimicrobial defence and immunoregulation. Thromb Haemost 2005; 94: 341-6.
• 15 Dehio M, Quebatte M, Foser S, Certa U. The transcriptional response of human endothelial cells to infection with Bartonella henselae is dominated by genes controlling innate immune responses, cell cycle, and vascular remodelling. Thromb Haemost 2005; 94: 347-61.