Innate Immunity continued:
Inflammation followed by
Toll like receptors
,Inflammation: a coordinated process designed
to recruit immune cells to fight infections and
promote repair.
If there is tissue
damage
Cellular order :1st: local macrophages: 2nd: neutrophils: 3rd monocytes
, Inflammation: a necessary process to fight infections
1. Pro-inflammatory mediators produced by macrophages and other cells
cause a cascade of signals resulting in activated local endothelial cells
that express more adhesion molecules.
2. Vascular diameters and permeability increase in the local vessels
due to lipid mediators such as prostaglandins, leukotrienes,
and cytokines like TNFa. This results in swelling.
Aspirin actually decreases prostaglandin release
by targetting COX-2, a needed biosynthetic enzyme for the pathway,
and can promote lipoxin production, which resolves inflammation.
3. Immune cells are recruited to the inflamed site, first neutrophils
and then monocytes by chemoattractants and the adhesion molecules
on the endothelia. Cells leave the blood vessels and migrate
into the tissue to fight infection at the site.
Inflammation followed by
Toll like receptors
,Inflammation: a coordinated process designed
to recruit immune cells to fight infections and
promote repair.
If there is tissue
damage
Cellular order :1st: local macrophages: 2nd: neutrophils: 3rd monocytes
, Inflammation: a necessary process to fight infections
1. Pro-inflammatory mediators produced by macrophages and other cells
cause a cascade of signals resulting in activated local endothelial cells
that express more adhesion molecules.
2. Vascular diameters and permeability increase in the local vessels
due to lipid mediators such as prostaglandins, leukotrienes,
and cytokines like TNFa. This results in swelling.
Aspirin actually decreases prostaglandin release
by targetting COX-2, a needed biosynthetic enzyme for the pathway,
and can promote lipoxin production, which resolves inflammation.
3. Immune cells are recruited to the inflamed site, first neutrophils
and then monocytes by chemoattractants and the adhesion molecules
on the endothelia. Cells leave the blood vessels and migrate
into the tissue to fight infection at the site.
