High blood levels of the chemokine eotaxin-1 (CCL11) have recently been associated with aging and dementia, as well as impaired memory and learning in humans. Importantly, eotaxin-1 was shown to pass the blood-brain-barrier (BBB) and has been identified as crucial mediator of decreased neurogenesis and cognitive impairment in young mice after being surgically connected to the vessel system of old animals in a parabiosis model.

It thus has to be assumed that differences in eotaxin-1 levels between blood donors and recipients might influence cognitive functions also in humans. However, it is unknown if eotaxin-1 is stable during processing and storage of transfusion blood components.

This study assesses eotaxin-1 concentrations in fresh-frozen plasma (FFP), erythrocyte concentrate (EC), and platelet concentrate (PC) in dependence of storage time as well as the donor’s age and gender.

Eotaxin-1 was measured in FFP (n = 168), EC (n = 160) and PC (n = 8) ready-to-use for transfusion employing a Q-Plex immunoassay for eotaxin-1. Absolute quantification of eotaxin-1 was performed with Q-view software.

Eotaxin-1 was consistently detected at a physiological level in FFP and EC but not PC. Eotaxin-1 levels were comparable in male and female donors but increased significantly with rising age of donors in both, FFP and EC. Furthermore, eotaxin-1 was not influenced by storage time of either blood component. Finally, eotaxin-1 is subject to only minor fluctuations within one donor over a longer period of time.

In the present study, we prove that eotaxin-1 is still detectable at a normal level in processed blood products ready for transfusion and its concentration greatly differs between donors in an age-dependent manner. Thus, transfusion of larger amounts of blood components from older donors to younger recipients may increase total eotaxin-1 blood levels of the recipient.

Based on the above mentioned findings, it is possible that such a sudden increase in eotaxin-1 might impair cognitive abilities of the recipient. In this context, it is known that a considerable proportion of patients exhibit a temporary or even permanent decline in cognitive performance after major surgery, a phenomenon called postoperative cognitive dysfunction (POCD).

The prevalence of POCD varies from 41% to 75% at 7 days to 18%–45% at 3 months postoperatively, depending on diagnosis criteria and surgery type studied. The underlying mechanisms are not understood, however increasing evidence indicates that an enhanced inflammatory response might cause POCD.

Intraoperative transfusion of ECs (>3 units) has been described as an independent risk factor for development of POCD. Considering eotaxin-1 as chemoattractant for neutrophils and its ability to pass the BBB, it is possible that high eotaxin-1 levels in FFP or EC from older donors might contribute to POCD in recipients.

Eotaxin-1 is detectable and stable in FFP and EC and increases with donor’s age. Considering the presumed involvement in aging and cognitive malfunction, differences in donor- and recipient eotaxin-1 levels might affect mental factors after blood transfusion.