Cellular exudate is formed during the second and the third phase of inflammation -- acute and chronic cellular response. During the former, neutrophils are prevalent, whereas mononuclear cells (macrophages and lymphocytes) overcome later. Cell composition of exudate differ not only depending on the phase of inflammation but also on the type of inflamed tissue and factors triggering inflammatory process. Central effector and regulatory functions in acute inflammation posses neutrophils. They are also dominant when a pyogenic bacterial infection or local deposition of immune complexes containing IgG are the cause of inflammation. Mononuclear phagocytes represent the main infiltrating cells in subacute and chronic phase of the majority of inflammatory reactions, and in the case of infection with intracellularly parasitizing microorganisms as well. Eosinophils and basophils are predominant when inflammation has been initiated by immediate alergic reactions or by parasites.
So, a number of different cell types are recruited into the area where damage has occured, and these are responsible for inactivation and removing of the invading infectious agents, for removing the damaged tissues, for inducing the formation of new tissue, and reconstructing the damaged cell matrix, including basement membranes and connective tissue. A new blood supply to the area is also established during the repair process.
Professional phagocytes (neutrophils, eosinophils, monocytes and tissue macrophages) are essential performing phagocytosis, lymphocytes are involved in the specific immune responses, endothelial cell in the regulation of leukocyte emigration from the blood into inflamed tissue and platelets with mast cells in the production od early phase mediators.
The accumulation of leukocytes in inflamed tissue results from adhesive interactions between leukocytes and endothelial cells within the microcirculation. These adhesive interactions and the excessive filtration of fluid and protein that accompanies an inflammatory response are largely confined to one region of the microvasculature -- postcapillary venules. The nature and magnitude of the leukocyte-endothelial cell adhesive interactions that take place within postcapillary venules are determined by a variety of factors, including expression of adhesion molecules on leukocytes and/or endothelial cells, products of leukocyte (superoxide and other ROI) and endothelial cell (nitric oxide) activation, and the physical forces generated by the movement of blood along the vessel wall. The contribution of different adhesion malecules to leukocyte rolling, adherence, and emigration in venules will be discussed later.
This process is similar for granulocytes, monocytes, and lymphocytes, only different chemotactic factors and cytokines may be involved in its initiation and control. The white blood cells leave the postcapillarly venule by extending pseudopodia between apposing endothelial cells and pulling themselves into the subendothelial space and the adjacent interstitial compartment. This complex event, which is often termed leukocyte extravasation, emigration, or diapedesis, is dependent not only on an array of cellular processes including adhesion molecule expression and activation, but also on cytoskeletal reorganization, and alteration in membrane fluidity.
