Allergic inflammatory response

Histamine contributes to the progression of allergic-inflammatory responses by enhancement of the secretion of proinflammatory cytokines like IL-la, IL-1(3, IL-6 as well as chemokines like RANTES or IL-8, both in several cell types and local tissues [26-29]. Endothelial cells express functional HRl and HR2 and increased adhesion molecule expression such as ICAM-1, VCAM-1 and P-selectin was demonstrated by histamine infusion via HRl [30-32]. Histamine regulates the expression of its own receptors on endothelial cells and influences the overall inflammatory reaction [33]. 

Eosinophilic granulocytes Destroy larger parasites and modulate allergic inflammatory responses 2x10 3-8h... 

Th2-type cytokines such as IL-4, IL-5, and IL-13 orchestrate a cascade of events during development of an allergic inflammatory response. This is demonstrated both clinically and in preclinical animal models (404, 405). IL-4 plays a critical role in the early commitment of ThO cells to Th2 cells and regulates IgE secretion by B-cells. It also induces V-CAM expression on endothelial cells, promotes eosinophilic inflammation, and increases airway mucus production. 

Remirez, D., Ledon, N., and Gonzalez, R. (2002). Role of histamine in the inhibitory effects of phycocyanin in experimental models of allergic inflammatory response. Mediators Inflamm. 11, 81-85. 

In another study, chitosan was confirmed to partially inhibit the secretion of both IL-8 and TNF-a from mast cells, and it was proposed that water-soluble chitosan has the potential to reduce the allergic inflammatory response (Kim et al. 2005). Since mast cells are necessary for allergic reactions and have been implicated in a number of neuroinflammatory diseases, chitosan nutraceu-ticals may help to prevent or alleviate some of these complications. 

The current descriptions of sensitivity and maximal response are best applied to secretion of histamine. However, a more complete understanding will require further information about the same parameters in the context of lipid and cytokine release. Both of these mediators are critical determinants of the allergic inflammatory response, so that understanding the extent to which new therapeutics need to suppress basophil and mast cell responsiveness will be dependent on new information regarding the relative roles of each of the secreted mediators. Recent studies have indicated that basophil sensitivity is very similar when viewed from the secretion of each of three classes of mediators. This means that if cell surface antigen-specific IgE is present at a density sufficient to initiate only 50% of the maximum histamine release, approximately 50% of the maximal secretion of IL-4 and LTC4 will also be obtained. It remains to be determined whether the equivalent suppression of secretion for each of the three classes of mediators will lead to equivalent reductions for the functional endpoints of the three different mediator classes. 

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