Novel Class of Drug Delivery Liposomes Fail to Trigger an Adverse Immune Response

A novel class of liposomes prepared from the artificial phospholipid Pad-PC-Pad releases drugs at the site of arterial blockage, and has been shown to avoid activation of deleterious immune responses.

One therapeutic approach for treatment of atherosclerosis is a liposome-based drug carrier system specifically targeting constricted arteries. Vesicles made from an artificial 1,3-diaminophospholipid are stable under static conditions but release their contents at elevated shear stress. These vesicles have a lenticular morphology, which potentially leads to instabilities along their equator. A model cardiovascular system based on polymer tubes and an external pump to represent shear stress in healthy and constricted vessels of the heart showed that drugs preferentially released from the vesicles in constricted vessels that had high shear stress.


While these liposomes are promising delivery containers, they are recognized as foreign by the immune system. Complement activation, an essential factor of the recognition, leads to adverse effects on the organism.

Investigators at the University of Basel (Switzerland) and the University of Fribourg (Switzerland) tested complement activation by liposomes formulated from the artificial phospholipid Pad-PC-Pad in vitro. They reported in the December 27, 2015, online edition of the journal Nanomedicine: Nanotechnology, Biology, and Medicine that no complement activation was detected in human sera and porcine plasma. In in-vivo experiments with three pigs, neither anaphylactic reactions nor other significant hemodynamic changes were observed even at comparably high liposome doses.

"The study shows that Pad-PC-Pad liposomes are not inducing direct or indirect anaphylactic reactions, even at high dosages", said senior author Dr. Bert Müller, professor of materials science in medicine at the University of Basel. "These are highly unexpected results could have a high impact of future treatments of atherosclerosis."

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University of Basel
University of Fribourg