yes, these inflammatory cells are alive....neutrophils,
lymphocytes, later the neutophils reduce in number and the
lymphocytes and macrophages predominate as the surface mucosal
cells break down and get phagocytozed..
If you take repeated biopsy sample during the formation of the
ulcer and look under the microscope, the first thing you will see
is dilatation of the capillaries beneath the mucosa. The
capillaries become engorged with blood (due to the effect of
cytokines like nitrous oxide etc), the neutrophils and lymphocytes
move to the sides of the blood stream...what we call margination.
Then these white blood cells roll along the endothelium (lining of
blood capilaries) slow down and stick to the endothelial cells.
This is due to the interaction of molecules on the surface of
inflammatory cells and endothelial cells (such as E- selectin on
the endothelial cells that have been activated by cytokines eg.
TNFalpha) interacting with PSGL1 on the inflammatory cells.
Finally, they stop and squeeze through the intercellular spaces
between endothelial cells to enter the tissue spaces, along with
serum fluid.
The dilation of blood vessels cause the redness in the area that
will eventually break down. As the fluid and inflammatory cells
exude out, the area becomes swollen and paler in the centre, whilst
the periphery which shows the vasodilatation remains red.
The exuded inflammatory cells are attracted there by cytokines such
as IL-1 (interleukin-1) and TNF alpha. They degranulate and release
the proteolytic enzymes that attack the surface epithelial cells,
which break down. As the inflammation proceeeds, lymphocytes (T
cells in the main and some studies suggest mainly gamma-delta T
cells) come in to the area with macrophages. They begin to mop up
and phagocytose the cell debris and dying epithelial cells. The
breadown down of surface epithelial cells result in the central
defect as the ulcer forms.
sorry very long and boring but you want details right?
