[Significance of vascular endothelium for specific functional behavior of nasal mucosa].
BACKGROUND
During the last decade the morphological structure of nasal blood vessels was understood as a functional basis for different physiological and immunological reactions.


RESULTS
Under normal conditions the vascular endothelium is involved in many activities including hemostasis, defense reactions, and angiogenesis during repair and pathological events. Most of the required components are synthesized by the endothelium itself, including extracellular matrix components, coagulation reactants, and growth factors. The complex vasculature of the human nasal mucosa plays an important role in the protection of the respiratory tract by generation of nasal fluid under normal and pathologic conditions. Increased plasma exudation in inflammatory processes including increased plasma protein concentrations binds cytokines, mediators, and cell release products and transports them to the respiratory lumen. During inflammation, endothelial cells stimulated by cytokines like TNF (tumor necrosis factor) regulate the recruitment of leukocytes by expression of certain surface proteins, called adhesion molecules. They also secrete chemokines like IL-8 (interleukin-8) and MCP (monocyte chemotactic protein) to increase the affinity of adhesion molecules, spread the leukocyte form to a flat, migrating one, and stimulate cell locomotion. Last but not least, endothelial cells may also act as antigen presenting cells (APC), although antigen presentation by endothelium is not responsible for the generalized homing of T-cells once the response is working.


CONCLUSIONS
The new scientific results on the functional behaviour of vascular endothelium have opened new perspectives for our understanding of nasal blood vessels; it might also stimulate and enable us to search for new therapeutical concepts based on these findings.
Grevers
G
G
Klinik und Poliklinik für Hals-, Nasen-und Ohrenkranke, Ludwig-Maximilians-Universität München.
Sturm
C
C
D002199:Capillary Permeability / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D004730:Endothelium, Vascular / Q000276:immunology* / Q000473:pathology; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D009297:Nasal Mucosa / Q000098:blood supply* / Q000276:immunology; D012220:Rhinitis / Q000276:immunology* / Q000473:pathology
D015815:Cell Adhesion Molecules; D016207:Cytokines; D018836:Inflammation Mediators