scholarly journals Studying macrophage activation in immune-privileged lens through CSF-1 protein intravitreal injection in mouse model

2022 ◽  
Vol 3 (1) ◽  
pp. 101060
Yuting Li ◽  
Francisca M. Acosta ◽  
Yumeng Quan ◽  
Zhen Li ◽  
Sumin Gu ◽  
2018 ◽  
Vol 141 (4) ◽  
pp. 1439-1449 ◽  
Giusi Prencipe ◽  
Ivan Caiello ◽  
Antonia Pascarella ◽  
Alexei A. Grom ◽  
Claudia Bracaglia ◽  

2020 ◽  
Vol 9 (7) ◽  
pp. 9 ◽  
Alison Heffer ◽  
Victor Wang ◽  
Jayanth Sridhar ◽  
Steven E. Feldon ◽  
Richard T. Libby ◽  

2014 ◽  
Vol 15 (1) ◽  
pp. 63 ◽  
Jun Hong ◽  
Yutein Chung ◽  
Jessica Steenrod ◽  
Qiang Chen ◽  
Jing Lei ◽  

2016 ◽  
Vol 62 (6) ◽  
pp. 425-431 ◽  
Teruyoshi TANAKA ◽  
Tatsuya MORIYAMA ◽  
Yukio KAWAMURA ◽  

2020 ◽  
Vol 11 (1) ◽  
Simone Torretta ◽  
Alessandra Scagliola ◽  
Luisa Ricci ◽  
Francesco Mainini ◽  
Sabrina Di Marco ◽  

AbstractD-mannose is a monosaccharide approximately a hundred times less abundant than glucose in human blood. Previous studies demonstrated that supraphysiological levels of D-mannose inhibit tumour growth and stimulate regulatory T cell differentiation. It is not known whether D-mannose metabolism affects the function of non-proliferative cells, such as inflammatory macrophages. Here, we show that D-mannose suppresses LPS-induced macrophage activation by impairing IL-1β production. In vivo, mannose administration improves survival in a mouse model of LPS-induced endotoxemia as well as decreases progression in a mouse model of DSS-induced colitis. Phosphomannose isomerase controls response of LPS-activated macrophages to D-mannose, which impairs glucose metabolism by raising intracellular mannose-6-phosphate levels. Such alterations result in the suppression of succinate-mediated HIF-1α activation, imposing a consequent reduction of LPS-induced Il1b expression. Disclosing an unrecognized metabolic hijack of macrophage activation, our study points towards safe D-mannose utilization as an effective intervention against inflammatory conditions.

2020 ◽  
Vol 21 (23) ◽  
pp. 9297
Mi Sun Sung ◽  
Myeong Ju Moon ◽  
Reju George Thomas ◽  
So Young Kim ◽  
Jun Sung Lee ◽  

Various neuroprotective agents have been studied for the treatment of retinal ganglion cell (RGC) diseases, but issues concerning the side effects of systemically administered drugs and the short retention time of intravitreally injected drugs limit their clinical applications. The current study aimed to evaluate the neuroprotective effects of intravitreally injected trichostatin A (TSA)-loaded liposomes in a mouse model of optic nerve crush (ONC) and determine whether TSA-loaded liposomes have therapeutic potential in RGC diseases. The histone deacetylase inhibitor, TSA, was incorporated into polyethylene glycolylated liposomes. C57BL/6J mice were treated with an intravitreal injection of TSA-loaded liposomes and liposomes loaded with a lipophilic fluorescent dye for tracking, immediately after ONC injury. The expression of macroglial and microglial cell markers (glial fibrillary acidic protein and ionized calcium binding adaptor molecule-1), RGC survival, and apoptosis were assessed. We found that the liposomes reached the inner retina. Their fluorescence was detected for up to 10 days after the intravitreal injection, with peak intensity at 3 days postinjection. Intravitreally administered TSA-loaded liposomes significantly decreased reactive gliosis and RGC apoptosis and increased RGC survival in a mouse model of ONC. Our results suggest that TSA-loaded liposomes may help in the treatment of various RGC diseases.

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