Public defence in Chemistry: Linnea Andersson

In order to receive the Zoom link for the thesis defense, please contact Faculty Administrator Linnéa Larsson: linnea.larsson@lnu.se

Abstract

As soon as blood leaves the human body, stress to the host´s protective
cellular and protein cascades begin. My thesis focuses on the immune
system, specifically the complement system and platelets, primarily known
for their hemostatic properties but also play a role in immune responses. The
core of this thesis is the interaction between the complement system and
platelets in platelet concentrates destined for transfusion. Storing blood
products, particularly platelet concentrates, presents challenges, including
the development of platelet storage lesions. These lesions involve a series
of biochemical, structural, and functional changes from when platelets are
collected to when they are transfused, potentially leading to impaired
platelet function and adverse transfusion reactions. For inventory
management, the oldest platelet concentrates are typically used first for
transfusion. Understanding the interplay between the complement system
and platelets during storage is crucial for improving the quality of platelet
concentrates for selecting optimal concentrates based on the indication. This
thesis includes several exploratory studies: one examining the complement
system and platelet function over storage time, another investigating the
impact of complement inhibition with the aim to reduce platelet storage
lesions, and a third exploring the ability of platelets to release mediators that
can modulate an immune response when supplemented to thrombocytopenic
blood. Additionally, one study examines the impact of blood collection tube
composition on complement functional and activation analysis. I found that
increased storage time was associated with increased complement
activation, increased platelet activation and attenuated platelet function.
However, there was no causal relationship between complement and platelet
activation since complement inhibition did not alter platelet activation or
function. Further, I found that platelets release mediators that could
modulate an inflammatory reaction, but the storage time had only minor
effect on the immunomodulatory effect. Last, I found that the composition
of blood collection tubes significantly affected complement activation.
While these findings may not immediately benefit patients, they provide
new insights into platelet concentrates, highlighting the role of the
complement system. Further research is needed to understand the
interaction between these components fully.