Activation of basophils by stem cell factor: comparison with insulin-like growth factor-I

Basophils are an active participant in the pathogenesis of local inflammation in allergic diseases such as asthma, but it is not fully known how basophil activation is regulated in inflamed tissue.

In order to clarify the control mechanisms of basophil activation in chronic inflammation and at remodeling sites, we analyzed the effects of fibroblast-derived cytokines, stem cell factor (SCF), and insulin-like growth factor-I (IGF-I) on basophils.

The effects of SCF and IGF-I on degranulation and surface activation marker expression by basophils were assessed and compared.

SCF enhanced human basophil histamine release elicited by some, but not all, secretagogues; degranulation in response to IgE- or FcepsilonRI-mediated stimulation and 12-o-tetradecanoyl-phorbol-13-acetate (TPA) was enhanced by SCF. SCF slightly enhanced ionophore A23187-induced histamine release by basophils from some donors, but it failed to affect the release elicited by monocyte chemoattractant protein-1 (MCP-1), formylmethionyl-leucyl-phenylalanine (FMLP) or C5a. The repertoire of secretagogues responsive to SCF was similar to that of IGF-I. Expression levels of both CD11b and CD69 markers were significantly enhanced by the combination of SCF and IGF-I.

These results suggest that SCF and IGF-I may modify the activation of basophils in a similar and/or synergistic fashion. Interaction of basophils with these cytokines might be involved in the pathogenesis of local inflammation and the remodeling process in asthma.