| dc.creator |
Gonzalo, José Ángel |
|
| dc.creator |
Lloyd, Clare M. |
|
| dc.creator |
Kremer, Leonor |
|
| dc.creator |
Finger, Elizabeth |
|
| dc.creator |
Martínez-Alonso, Carlos |
|
| dc.creator |
Siegelman, M.H. |
|
| dc.creator |
Cybulsky, Myron |
|
| dc.creator |
Gutiérrez Ramos, José Carlos |
|
| dc.date |
2008-04-16T10:46:04Z |
|
| dc.date |
2008-04-16T10:46:04Z |
|
| dc.date |
1996-11 |
|
| dc.date.accessioned |
2017-01-31T01:02:26Z |
|
| dc.date.available |
2017-01-31T01:02:26Z |
|
| dc.identifier |
The Journal of Clinical Investigation, vol. 98(10), pp. 2332-2345, (1996) |
|
| dc.identifier |
0021-9738 |
|
| dc.identifier |
http://hdl.handle.net/10261/3617 |
|
| dc.identifier |
10.1172/JCI119045 |
|
| dc.identifier.uri |
http://dspace.mediu.edu.my:8181/xmlui/handle/10261/3617 |
|
| dc.description |
Eosinophil accumulation is a distinctive feature of lung allergic inflammation. Here, we have used a mouse model of
OVA (ovalbumin)-induced pulmonary eosinophilia to study the cellular and molecular mechanisms for this selective recruitment of eosinophils to the airways. In this model there was an early accumulation of infiltrating monocytes/macrophages in the lung during the OVA treatment, whereas the increase in infiltrating T-lymphocytes paralleled the accumulation of eosinophils. The kinetics of accumulation of these three leukocyte subtypes correlated with the levels of
mRNA expression of the chemokines monocyte chemotactic peptide-1/JE, eotaxin, and RANTES (regulated upon activation
in normal T cells expressed and secreted), suggesting their involvement in the recruitment of these leukocytes.
Furthermore, blockade of eotaxin with specific antibodies in vivo reduced the accumulation of eosinophils in the lung in
response to OVA by half. Mature CD4
1 T-lymphocytes were absolutely required for OVA-induced eosinophil accumulation
since lung eosinophilia was prevented in CD4
1 -deficient mice. However, these cells were neither the main producers of the major eosinophilic chemokines eotaxin,
RANTES, or MIP-1 a, nor did they regulate the expression of these chemokines. Rather, the presence of CD4 1 T cells
was necessary for enhancement of VCAM-1 (vascular cell adhesion molecule-1) expression in the lung during allergic
inflammation induced by the OVA treatment. In support of this, mice genetically deficient for VCAM-1 and intercellular
adhesion molecule-1 failed to develop pulmonary eosinophilia.
Selective eosinophilic recruitment during lung allergic inflammation results from a sequential accumulation of certain leukocyte types, particularly T cells, and relies on the presence of both eosinophilic chemoattractants and adhesion
receptors. |
|
| dc.description |
Peer reviewed |
|
| dc.format |
26512709 bytes |
|
| dc.format |
application/pdf |
|
| dc.language |
eng |
|
| dc.publisher |
American Society for Clinical Investigation |
|
| dc.rights |
openAccess |
|
| dc.subject |
Lung eosinophilia |
|
| dc.subject |
Leukocytes |
|
| dc.subject |
Chemotactic cytokines |
|
| dc.subject |
Integrins |
|
| dc.subject |
Selectins |
|
| dc.title |
Eosinophil recruitment to the lung in a murine model of allergic inflammation : the role of T Cells, chemokines, and adhesion receptors |
|
| dc.type |
Artículo |
|