Eosinophil-endothelial interaction

A large number of cells are involved in the immune response and all are derived fiom the multipotential stem cells of the bone marrow. The predominant cell is the lymphocyte but monocytes-macrophages, endothelial cells, eosinophils and mast cells are also involved with certain immune responses. The two types of immunity (humoral and cell-mediated) are dependent on two distinct populations of lymphocytes, the B cells and the T cells respectively. Both the humoral and the cell-mediated systems interact to achieve an effective immune response. 

The predominance of inflammatory changes in the fascia suggests that mediators produced by mesenchymal cells (fibroblasts and endothelial cells) may also play a role in the pathogenesis. For example, fibroblasts augment IL-5-dependent eosinophil survival and stimulate conversion to the hypodense phenotype. Fibroblasts can also produce IL-8, which recruits neutrophils and lymphocytes when injected in vivo. Thus, one can speculate that the etiologic agent interacts with these cells to stimulate release of inflammatory mediators and increase collagen synthesis. 

Although absent from the surface of resting endothelial cells in culture the expression of VCAM-1 is induced by IL-1, IL-4, and TNF-a but not IFN-y.44-46 Endothelial VCAM-1 supports the adhesion of lymphocytes and monocytes (but not neutrophils) through interaction with VLA-4,45 47 and this recognition mechanism could lead to the accumulation of mononuclear cells during the transition from acute to chronic inflammation. It appears that VCAM-1 also underlies eosinophil and basophil adhesion to activated endothelium.48... 

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