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Research of Asthma




Asthma is associated with chronic, T cell-mediated inflammation of the bronchial mucosa characterized by a striking and relatively specific influx of eosinophils. It’s believe that Eosinophil products cause much of the bronchial mucosal damage which is thought ultimately to give rise to clinical symptoms. IgE-mediated or otherwise,release of mast cell and basophil products is additionally thought to cause acute exacerbation of asthma symptoms. 

One fundamental aspect of asthma research has been to determine the mechanism of this specific eosinophil influx. It’s thought that local release of cytokines from‘Th2-type’activated T cells  pivotal to this process, particularly IL-5, which acts exclusively on eosinophils and their committed precursors, but also IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) which act on eosinophils but less specifically.Since these cytokines can promote maturation of eosinophils in the bone marrow, increased adherence of eosinophils to vascular endothelium, and priming, activation and prolonged survival of these cells in the tissues. One function not clearly attributable to these cytokines is the induction of diapedesis of cells across vascular endothelium. This role is potentially ideally filled by the CC chemokines. In particular, eotaxin and eotaxin-2 may attract eosinophils, basophils and‘Th2-type’T cells into tissues, and specifically so via interaction with the CCR3 receptor.

There exists considerable evidence in support of this cooperation between eotaxin and IL-5 in the mechanism of specific eosinophil influx in the tissues from studies on animals.Eotaxin, when injected directly into the arterial supply of the guinea pig femoral bone marrow, caused a rapid and selective release of eosinophils into the draining vein. Eosinophil progenitor cells, which have recently also been shown to express CCR3, were also released, an effect not observed with IL-5. Eotaxin administered subcutaneously to IL-5 gene-deleted mice failed to evoke local eosinophil accumulation unless exogenous IL-5 was administered concurrently. 

ELISA(enzyme-linked immunosorbent assay) is a method for detecting the concentration of some kind antigen or antibody,such as eotaxin and IL-5, using the characteristic of specific binding between antigen-antibody.The method is suitable for determination of cell culture supernatant, serum, plasma,tissue fluid, and urine samples. Meretciel provide quality ELISA kits for R&D,can use to study of Asthma.

The mechanisms by which eotaxin evokes this ‘two-way traffic’ of eosinophils (into tissues but out of the bone marrow) are as yet poorly defined, but these may at least partly involve interactions of β1- and β2-integrin adhesion molecules (CD11b/CD18, VLA-4) on eosinophils with counter-receptors :intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) on local endotlielial cells. Interestingly, IL-4 may also attract eosinophils through secondary eotaxin release.


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