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Macrophages, epithelial cells of the CCL2 help rhinovirus induced high reactivity and inflammation i

Human rhinovirus (HRV) infection that causes disease in asthma attack reduce air, but not in healthy individuals. However, the mechanisms underlying the is still fully understood. We assume that the nuclear drive allergy environment can improve the HRV induced CC chemokine production, which can lead to asthma attacks. Ovalbumin all (OVA) sensitization and challenges vaccinated mice showed a significant increase HRV express lung CCL2 / MCP 1 and aram/MIP - 1 β, CCL7 / MCP 3, CCL19 / MIP - 3 beta and CCL20 / MIP3 α alone than mice with eggs. Inhibiting the CCL2 and neutralizing antibody declined obviously, and HRV induced air inflammation and high reactivity in treatment of mice eggs. Immunohistochemical staining display colocalization CCL2 HRV in epithelial cells and CD68 - positive macrophages and flow cytometry show an increase in the CCL2 (+), CD11b (+) cell lung eggs treatment, HRV infection of mouse. And from a naive mice lung macrophages, macrophages from mice expressed significantly more eggs exposure in response to HRV infection CCL2 in vitro. Pretreatment of mouse and human BEAS - 2 b pulmonary macrophages bronchial epithelial cells and il 4 and il and increase HRV induced the CCL2 expression, and mouse lung macrophages from il 4 receptor knockout mice showed that decreasing response HRV CCL2 expression that come into contact with these individual nucleus cell factor play a role change HRV response. Finally, bronchial alveolar macrophage from children with asthma were described in vitro more CCL2 contact ratio from the asthma patients HRV cell. We come to the conclusion that the epithelial cells of the CCL2 production and macrophage help HRV induced airway hyperresponsiveness and inflammation in a mouse model of allergic aviation disease, may play a role in the HRV induced asthma.
11.12.12 13:38
 


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