Immunosuppressive dead cell as lung-targeting vehicle and cytokine absorption material for cytokine storm attenuation of pneumonia

Effectively controlling cytokine storm is important to reduce the mortality of severe pneumonia. In this work a bio-functional dead cell was engineered by one-time quick shock of live immune cells in liquid nitrogen, and the obtained immunosuppressive dead cell could server as both lung-targeting ve...

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Published inMaterials today bio Vol. 20; p. 100684
Main Authors Ci, Tianyuan, Xiong, Yaoxuan, Zhang, Jinniu, Zang, Jing, Feng, Nianping
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.06.2023
Elsevier
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Summary:Effectively controlling cytokine storm is important to reduce the mortality of severe pneumonia. In this work a bio-functional dead cell was engineered by one-time quick shock of live immune cells in liquid nitrogen, and the obtained immunosuppressive dead cell could server as both lung-targeting vehicle and cytokine absorption material. After loading the anti-inflammatory drugs of dexamethasone (DEX) and baicalin (BAI), the drug-loaded dead cell (DEX&BAI/Dead cell) could first passively target to the lung after intravenous administration and quickly release the drugs under high shearing stress of pulmonary capillaries, realizing drug enrichment in the lung. Then, the immunosuppressive dead cell acted as the camouflage of normal immune cells with various cytokine receptors exposing on their surface, to “capture” the cytokines and further reduce the state of inflammation. With above formulation design, a synergic anti-inflammatory effect between drugs and carrier could be achieved. In a lipopolysaccharide-induced pneumonia mice model, this system could calm down the cytokine storm with high efficacy and elongate the survival of mice. Effectively controlling cytokine storm is important to reduce the mortality of severe pneumonia. An immunosuppressive dead cell was engineered as lung targeting vehicle and mixed antibodies of cytokines to achieve the synergetic anti-inflammatory effects and attenuate the cytokine storm. [Display omitted]
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These authors contributed equally to this work.
ISSN:2590-0064
2590-0064
DOI:10.1016/j.mtbio.2023.100684