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J Inflamm (Lond). 2011 Aug 11;8:19. doi: 10.1186/1476-9255-8-19.

Triple selectin knockout (ELP-/-) mice fail to develop OVA-induced acute asthma phenotype.

Author information

1
Division of Hematology, Department of Medicine, University of Washington, 1959 NE Pacific Street, Seattle, WA 98195, USA. enarb1@gmail.com.

Abstract

OBJECTIVE:

The recruitment of leukocytes from circulation to sites of inflammation requires several families of adhesion molecules among which are selectins expressed on a variety of cells. In addition, they have also been shown to play key roles in the activation of cells in inflammation.

METHODS:

To explore the collective role of E-, L-, and P- selectins in OVA-induced Th2 mediated response in acute asthma pathophysiology, ELP-/- mice were used and compared with age-matched wildtype (WT).

RESULTS:

Asthma phenotype was assessed by measuring pulmonary function, inflammation and OVA-specific serum IgE, which were completely abrogated in ELP-/- mice. Adoptive transfer of sensitized L selectin+CD4+ T cells into naïve ELP-/- mice which post-OVA challenge, developed asthma, suggesting that L-selectin may be critically involved in the onset of Th2 response in asthma. Tissue resident ELP-deficient cells were otherwise functionally competent as proved by normal proliferative response.

CONCLUSIONS:

Comparative studies between ELP-/- and WT mice uncovered functional roles of these three integrins in inflammatory response in allergic asthma. All three selectins seem to impede inflammatory migration while only L-selectin also possibly regulates activation of specific T cell subsets in lung and airways.

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