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

Authors: English, K  Brady, C  Corcoran, P  Cassidy, JP  Mahon, BP 
Citation: English K, etal., Immunol Lett. 2006 Mar 15;103(2):92-100. Epub 2005 Oct 21.
Pubmed: (View Article at PubMed) PMID:16290206
DOI: Full-text: DOI:10.1016/j.imlet.2005.09.011

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-kappaB, including IL-1beta 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.

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CRRD Object Information
CRRD ID: 4892195
Created: 2011-02-09
Species: All species
Last Modified: 2011-02-09
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.