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Publication : Siglec-F-dependent negative regulation of allergen-induced eosinophilia depends critically on the experimental model.

First Author  McMillan SJ Year  2014
Journal  Immunol Lett Volume  160
Issue  1 Pages  11-16
PubMed ID  24698729 Mgi Jnum  J:288980
Mgi Id  MGI:6435607 Doi  10.1016/j.imlet.2014.03.008
Citation  McMillan SJ, et al. (2014) Siglec-F-dependent negative regulation of allergen-induced eosinophilia depends critically on the experimental model. Immunol Lett 160(1):11-16
abstractText  Siglec-8 and siglec-F are paralogous membrane proteins expressed on human and murine eosinophils respectively. They bind similar sialylated and sulphated glycans and mediate eosinophil apoptosis when cross-linked with antibodies or glycan ligands. In models of allergic eosinophilic airway inflammation, siglec-F was shown previously to be important for negatively regulating eosinophilia. It was proposed that this was due to siglec-F-dependent apoptosis, triggered via engagement with ligands that are upregulated on bronchial epithelium. Our aim was to further investigate the functions of siglec-F by comparing two commonly used models of ovalbumin-induced airway inflammation that differ in the dose and route of administration of ovalbumin. In confirmation of published results, siglec-F-deficient mice had enhanced lung tissue eosinophilia in response to intranasal ovalbumin delivered every other day. However, following aerosolised ovalbumin delivered daily, there was no influence of siglec-F deficiency on lung eosinophilia. Expression of siglec-F ligands in lung tissues was similar in both models of allergen induced inflammation. These data demonstrate that siglec-F-dependent regulation of eosinophilia is subtle and depends critically on the model used. The findings also indicate that mechanisms other than ligand-induced apoptosis may be important in siglec-F-dependent suppression of eosinophilia.
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