Journal
BLOOD
Volume 108, Issue 5, Pages 1588-1594Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2005-12-012781
Keywords
-
Categories
Funding
- NHLBI NIH HHS [HL 036110] Funding Source: Medline
- NIAID NIH HHS [AI 057991, AI 031599, AI 052353, AI 047379, AI 048802, R01 AI047379] Funding Source: Medline
Ask authors/readers for more resources
Normal mouse lungs lack appreciable numbers of mast cells (MCs) or MC progenitors (MCp's), yet the appearance of mature MCs in the tracheobronchial epithelial surface is a characteristic of allergic, T-cell-dependent pulmonary inflammation. We hypothesized that pulmonary inflammation would recruit MCp's to inflamed lungs and that this recruitment would be regulated by distinct adhesion pathways. Oval bumin-sensitized and challenged mice had a greater than 28-fold increase in the number of MCp's in the lungs. In mice lacking endothelial vascular cell adhesion molecule 1 (VCAM-1) and in wild-type mice administered blocking monoclonal antibody (mAb) to VCAM-1 but not to mucosal addressin CAM-1 (MadCAM-1), recruitment of MCp's to the inflamed lung was reduced by greater than 75%. Analysis of the integrin receptors for VCAM-1 showed that in beta 7 integrin-deficient mice, recruitment was reduced 73% relative to wild-type controls, and in either BALB/c or C57B/L6 mice, mAb blocking of alpha 4, beta 1, or beta 7 integrins inhibited the recruitment of MCp's to the inflamed lung. Thus, VCAM-1 interactions with both a4 beta 1 and alpha 4 beta 7 integrins are essential for the recruitment and expansion of the MCp populations in the lung during antigen-induced pulmonary inflammation. Furthermore, the MCp is currently unique among inflammatory cells in its partial dependence on a4 beta 7 integrins for lung recruitment.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available