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Abstract

It has been a fantasy that nanomedicine may significantly improve the delivery efficiency of medicine into the targets. The reality is harsh, as numerous clinical data have suggested that only modest improvement was observed. Scientists are searching for better ways of delivering medicine in a more precise manner. Cells are a basic unit of living organisms and using them as drug carriers has unique advantages. For instance, it can significantly improve the targeting efficiency due to the homing effects of selected cells or improve the systemic circulation. There are currently two strategies to construct cell-hitchhiking delivery systems. One is to directly phagocytose drugs (including nano-drugs) via endocytosis, and the other is to use covalent bonds or biological ligand-receptor interactions to conjugate nanomedicine to the surface of live cells. However, the cells that phagocytize medicines may degrade the drug before reaching the target. Covalent binding involves a complex synthetic process on the cell surface, which may impair the physiological function of the carrier cells. The ligand-receptor interaction is often limited to specific cells, and competitive ligand displacement occurs in vivo as well. During the past a couple of years, we have developed several supramolecular approaches to tackle these above-mentioned issues and to enable targeted delivery of various nanomedicines to inflammatory tissues (including solid tumors), driven by the inflammatory tropism of immune cells. We show that these unique systems may significantly improve the delivery efficiency of medicine into the targeted tissues and effectively treat several inflammatory diseases including acute pneumonia and atherosclerosis, and solid tumors such as melanoma.