Two waves of spontaneous fetal loss occur during commercial swine pregnancy; one during early and the other during mid-pregnancy. Decreased angiogenesis and increased pro-inflammatory cytokines have been found at arresting fetal attachment sites. However, levels of chemokines, small molecules responsible for chemoattraction, and their regulators, decoy receptors, are not reported. I hypothesized that decoy receptors contribute to fetal demise by altering endometrial cell trafficking via chemokine degradation. Select chemokines and decoy receptors were quantified at the maternal-fetal interface. Transcript number of homeostatic decoy receptor 'CCX CKR' was significantly higher in arresting gd50 tissues, compared with healthy gd50 tissues. Immunohistological localization of CCL4, CCX CKR, and D6 confirmed their expression in endometrium. The differential expression of chemokines and decoy receptors between healthy and arresting attachment sites may contribute to conceptus fate by altering the ratios of recruited cell types at the maternal-fetal interface.