目前，研究者對於細胞內細菌介導的抗生素耐藥性在慢性和復發性感染中所發揮的關鍵作用還了解不足。由於受感染細胞會阻止藥物滲透，並且保留在細菌部位的藥物濃度較低，因此常規的抗生素治療往往效果不佳，需要開發新的策略以用於細胞內抗感染治療。
(A) Preparation of the targeted intracellular drug delivery nanosystem by co-assembly of TPE-PMAMA-PLAMA and PCL-b-PAAPBA. (B) Design and predicted mechanism of the nanosystem to kill intracellular bacteria residing inside macrophages.
Fig 1. (A) Schematic illustration of specific entry of glycosylated nanoparticles into macrophages. (B) Confocal microscopy observations of RAW264.7 cells after incubation with free PI, r/40@PI NPs, and b/40@PI NPs, using the same dose of PI, for 1 and 3h. (C) Mean fluorescence intensities of PI in RAW264.7 cells calculated by software Image J after various treatments. (D–I) Fluorescence intensity of TPE (D, F, and H) and PI (E, G, and I) in RAW264.7 cells determined by flow cytometry after incubation with free PI, T-b/40@PI NPs, and T-r/40@PI NPs for 3h using the same dose of PI with or without 30 min pretreatment with a competitive inhibitor (mannosamine or galactosamine hydrochloride, 100 mM). (J and K) Relative geometric mean fluorescence intensities (GMFI) of (J) TPE and (K) PI in RAW264.7 cells after incubation.
Fig 2. (A) Schematic illustration of the experimental design to evaluate the therapeutic effect of the NPs. (B) CFU counts of remaining S. aureus strains in the infected posterior right thigh muscle tissue separated from healthy Balb/c mice and micebefore and after treatment with PBS, free CLA (7.5 mg/kg), and T-r/40@CLANPs (T-r/40 NPs: 20 mg/kg; CLA: 7.5 mg/kg) twice per day for 2 days. (C) Quantitative analysis of bacterial CFUs in the various groups. Inflammation-related expression of (D) TNF-α and (E) IL-6 in S. aureus muscle-infected mice of the various groups.
來源：Biomaterials雜誌
論文鏈接
https://www.sciencedirect.com/science/article/abs/pii/S0142961221006657
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