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University of California, San Diego

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Nat. Commun., Published:17 May 2018, 9, Article number: 1969 | doi:10.1038/s41467-018-04390-7 Immunogene therapy with fusogenic nanoparticles modulates macrophage response to Staphylococcus aureus

Byungji Kim¹, Hong-Bo Pang^2,3, Jinyoung Kang⁴, Ji-Ho Park⁵, Erkki Ruoslahti^2,6 & Michael J. Sailor^1,4,7,*
¹ Materials Science and Engineering Program, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. ² Cancer Research Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California 92037, USA. ³ Department of Pharmaceutics, University of Minnesota, Minneapolis, Minnesota 55455, USA. ⁴ Department of Nanoengineering, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. ⁵ Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.⁶ Center for Nanomedicine and Department of Cell, Molecular and Developmental Biology, University of California, Santa Barbara, Santa Barbara, California 93106-9610, USA. ⁷Department of Chemistry and Biochemistry, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA.

These authors contributed equally: Byungji Kim, Hong-Bo Pang.
^*Correspondence and requests for materials should be addressed to M.J.S.

Abstract

The incidence of adverse effects and pathogen resistance encountered with small molecule antibiotics is increasing. As such, there is mounting focus on immunogene therapy to augment the immune system’s response to infection and accelerate healing. A major obstacle to in vivo gene delivery is that the primary uptake pathway, cellular endocytosis, results in extracellular excretion and lysosomal degradation of genetic material. Here we show a nanosystem that bypasses endocytosis and achieves potent gene knockdown efficacy. Porous silicon nanoparticles containing an outer sheath of homing peptides and fusogenic liposome selectively target macrophages and directly introduce an oligonucleotide payload into the cytosol. Highly effective knockdown of the proinflammatory macrophage marker IRF5 enhances the clearance capability of macrophages and improves survival in a mouse model of Staphyloccocus aureus pneumonia.

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형식Research article
게재일2018년 05월 (BRIC 등록일 2018-05-30)
연구진국내+국외 연구진
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