DEMO DEMOInflammatory Cell Accumulation
Neutrophil/ endothelial cell interactions have been extensively studied in vivo. The extravascular accumulation of other leukocytes. Cells adhere as a consequence of interactions between adhesive glycoproteins which can be expressed initially on either the endothelial cell or the leukocyte itself. Known chemotactic factors also induce neutrophil-dependent oedema formation, they are IL-8, C5a, FMLP and LTB4. These mostly act via specific neutrophil receptors to activate the integrin adhesive glycoproteins (e.g. CD18 on neutrophils). Other adhesive glycoproteins (e.g. L-selectin) are also considered to play an important role in the rolling /adhesion process.
Note that oedema formation is thought to occur at an early time point in the adhesion/emigration process. Certain agents, e.g., interleukin-1 and tumour necrosis factor (TNF) act by stimulating endothelial cells to express adhesive glycoproteins (ICAMs and E-selectin; this is dependent on protein synthesis and thus slow in onset). This leads to a slow accumulation of neutrophils in vivo with less oedema formation. However in in vitro assays of stimulated neutrophil movement where endothelial cells are absent (e.g.the Boyden chamber chemotaxis assay) they are inactive.