Brucella abortus-activated microglia induce neuronal death through primary phagocytosis

Glia ◽  
2017 ◽  
Vol 65 (7) ◽  
pp. 1137-1151 ◽  
Author(s):  
Ana M. Rodríguez ◽  
M. Victoria Delpino ◽  
M. Cruz Miraglia ◽  
Miriam M. Costa Franco ◽  
Paula Barrionuevo ◽  
...  
2013 ◽  
Vol 43 (11) ◽  
pp. 2854-2865 ◽  
Author(s):  
Hung Chuan Pan ◽  
Cheng Ning Yang ◽  
Yi Wen Hung ◽  
Wen Jane Lee ◽  
Hsing Ru Tien ◽  
...  

2013 ◽  
Vol 236 ◽  
pp. 270-282 ◽  
Author(s):  
Ya-Nan Zhao ◽  
Fang Wang ◽  
Yan-Xia Fan ◽  
Guan-Fang Ping ◽  
Jing-Yu Yang ◽  
...  

2000 ◽  
Vol 276 (16) ◽  
pp. 13113-13120 ◽  
Author(s):  
Jaroslava Ciesielski-Treska ◽  
Gabrielle Ulrich ◽  
Sylvette Chasserot-Golaz ◽  
Jean Zwiller ◽  
Marie-Odile Revel ◽  
...  

Glia ◽  
2007 ◽  
Vol 55 (5) ◽  
pp. 483-496 ◽  
Author(s):  
Ayan Ghoshal ◽  
Sulagna Das ◽  
Soumya Ghosh ◽  
Manoj Kumar Mishra ◽  
Vivek Sharma ◽  
...  

2013 ◽  
Vol 33 (10) ◽  
pp. 1574-1581 ◽  
Author(s):  
Jianming Wang ◽  
Tetsuhiro Fujiyoshi ◽  
Yasuharu Kosaka ◽  
Jonathan D Raybuck ◽  
K Matthew Lattal ◽  
...  

Cardiac arrest (CA) causes hippocampal neuronal death that frequently leads to severe loss of memory function in survivors. No specific treatment is available to reduce neuronal death and improve functional outcome. The brain's inflammatory response to ischemia can exacerbate injury and provides a potential treatment target. We hypothesized that microglia are activated by CA and contribute to neuronal loss. We used a mouse model to determine whether pharmacologic inhibition of the proinflammatory microglial enzyme soluble epoxide hydrolase (sEH) after CA alters microglial activation and neuronal death. The sEH inhibitor 4-phenylchalcone oxide (4-PCO) was administered after successful cardiopulmonary resuscitation (CPR). The 4-PCO treatment significantly reduced neuronal death and improved memory function after CA/CPR. We found early activation of microglia and increased expression of inflammatory tumor necrosis factor (TNF)-α and interleukin (IL)-1β in the hippocampus after CA/CPR, which was unchanged after 4-PCO treatment, while expression of antiinflammatory IL-10 increased significantly. We conclude that sEH inhibition after CA/CPR can alter the transcription profile in activated microglia to selectively induce antiinflammatory and neuroprotective IL-10 and reduce subsequent neuronal death. Switching microglial gene expression toward a neuroprotective phenotype is a promising new therapeutic approach for ischemic brain injury.


2016 ◽  
Vol 9 (2) ◽  
pp. 282-291
Author(s):  
Letícia Ribeiro ◽  
Cristiane Batassini ◽  
Roberta Bristot Silvestrin ◽  
Lisiane Bizarro ◽  
Tadeu Mello e Souza ◽  
...  
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