Molecular interactions between gold nanoparticles and model cell membranes

2015 ◽  
Vol 17 (15) ◽  
pp. 9873-9884 ◽  
Author(s):  
Peipei Hu ◽  
Xiaoxian Zhang ◽  
Chi Zhang ◽  
Zhan Chen

Direct observations of the lipid flip-flop induced by Au NP – model mammalian cell membrane interactions.

Soft Matter ◽  
2012 ◽  
Vol 8 (20) ◽  
pp. 5501 ◽  
Author(s):  
Seunghwan Jeong ◽  
Sung Ho Ha ◽  
Sang-Hyun Han ◽  
Min-Cheol Lim ◽  
Sun Min Kim ◽  
...  

2018 ◽  
Vol 61 (9-11) ◽  
pp. 1148-1162 ◽  
Author(s):  
Peipei Hu ◽  
Xiaoxian Zhang ◽  
Yaoxin Li ◽  
Cayla Pichan ◽  
Zhan Chen

2012 ◽  
Vol 46 (3) ◽  
pp. 1869-1876 ◽  
Author(s):  
Wen-Che Hou ◽  
Babak Yaghoubi Moghadam ◽  
Charlie Corredor ◽  
Paul Westerhoff ◽  
Jonathan D. Posner

Langmuir ◽  
2014 ◽  
Vol 30 (28) ◽  
pp. 8491-8499 ◽  
Author(s):  
Fu-Gen Wu ◽  
Pei Yang ◽  
Chi Zhang ◽  
Bolin Li ◽  
Xiaofeng Han ◽  
...  

2014 ◽  
Vol 106 (2) ◽  
pp. 286a
Author(s):  
Katie Brennan ◽  
Luke Cuculis ◽  
Shelli L. Frey

2020 ◽  
Vol 16 (12) ◽  
pp. e1009119
Author(s):  
Jamie L. Dombach ◽  
Joaquin L. J. Quintana ◽  
Toni A. Nagy ◽  
Chun Wan ◽  
Amy L. Crooks ◽  
...  

Infections caused by Gram-negative bacteria are difficult to fight because these pathogens exclude or expel many clinical antibiotics and host defense molecules. However, mammals have evolved a substantial immune arsenal that weakens pathogen defenses, suggesting the feasibility of developing therapies that work in concert with innate immunity to kill Gram-negative bacteria. Using chemical genetics, we recently identified a small molecule, JD1, that kills Salmonella enterica serovar Typhimurium (S. Typhimurium) residing within macrophages. JD1 is not antibacterial in standard microbiological media, but rapidly inhibits growth and curtails bacterial survival under broth conditions that compromise the outer membrane or reduce efflux pump activity. Using a combination of cellular indicators and super resolution microscopy, we found that JD1 damaged bacterial cytoplasmic membranes by increasing fluidity, disrupting barrier function, and causing the formation of membrane distortions. We quantified macrophage cell membrane integrity and mitochondrial membrane potential and found that disruption of eukaryotic cell membranes required approximately 30-fold more JD1 than was needed to kill bacteria in macrophages. Moreover, JD1 preferentially damaged liposomes with compositions similar to E. coli inner membranes versus mammalian cell membranes. Cholesterol, a component of mammalian cell membranes, was protective in the presence of neutral lipids. In mice, intraperitoneal administration of JD1 reduced tissue colonization by S. Typhimurium. These observations indicate that during infection, JD1 gains access to and disrupts the cytoplasmic membrane of Gram-negative bacteria, and that neutral lipids and cholesterol protect mammalian membranes from JD1-mediated damage. Thus, it may be possible to develop therapeutics that exploit host innate immunity to gain access to Gram-negative bacteria and then preferentially damage the bacterial cell membrane over host membranes.


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