This was based on the proximity of the selectin gene cluster to a putative mastitis-related quantitative trait locus (QTL), the up-regulation of SELL and SELP in the mammary gland following experimental infection with either S. uberis or E. coli and the established role of selectins in granulocyte diapedesis during inflammation (reviewed by Chen et al. [60]). This evidence concerns the gene SELP and infection.