Inflammation of the respiratory tract is associated with CCL28 and CCR10 expression in a murine model of allergic asthma

被引:31
作者
English, K
Brady, C
Corcoran, P
Cassidy, JP
Mahon, BP [1 ]
机构
[1] Inst Immunol, Mucosal Immunol Lab, NUI Maynooth, Kildare, Ireland
[2] Univ Coll Dublin, Dept Vet Pathol, Dublin 2, Ireland
基金
英国惠康基金;
关键词
CCL28; IL-1; beta; oncostatin M; CCR10; eosinophiI;
D O I
10.1016/j.imlet.2005.09.011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Mouse models and in vitro cell culture were used to examine airway expression of the mucosal chemokine CCL28. Low levels of constitutively expressed mRNA were observed in transformed murine epithelial cells, but high levels could be induced by stimulation. Cytokines that signal through NF-kappa B, including IL-1 beta and TNF-alpha or via JAK-STAT pathway including oncostatin M induced CCL28 in airway epithelial cells in vitro. Immunohistochemistry of murine airway tissue revealed that constitutive expression of CCL28 protein in vivo was low and not ubiquitous. However, abundant expression was detected in epithelia and lymphoid aggregates following allergic sensitization and challenge with ovalbumin. This was accompanied by increased detection of cells expressing CCR10 protein and mRNA in inflamed airways. Taken together, these data support a role for CCL28 in contributing to allergen driven airway pathologies, show that proinflammatory cytokines can induce this signal and suggest a role for CCR10 expressing cells in airway inflammation. (C) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:92 / 100
页数:9
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