In vivo effects of adding singular or combined anti-oxidative vitamins and/or minerals to diets on the immune system of tilapia (Oreochromis hybrids) peripheral blood monocyte-derived, anterior kidney-derived, and spleen-derived macrophages

2007 ◽  
Vol 115 (1-2) ◽  
pp. 87-99 ◽  
Author(s):  
Shao-Wen Hung ◽  
Ching-Yu Tu ◽  
Way-Shyan Wang
2021 ◽  
Author(s):  
Bo-Wei Zhou ◽  
Fang-Ling Zhang ◽  
Wen-Juan Zhang ◽  
xiao Yang ◽  
Zhi-Wen Yao ◽  
...  

Abstract Background:Propofol is a widely used anesthetic and sedative, which has been reported to exert an anti-inflammatory effect. TLR4 plays a critical role in coordinating the immuno-inflammatory response during sepsis. Whether propofol can act as an immunomodulator through regulating TLR4 are still unclear. In view of its potential as a sepsis therapy, we investigated the mechanisms underlying the immunomodulatory activity of propofol.Methods: The effects of propofol on TLR4 and Rab5a (a master regulator involved in intracellular trafficking of immune factors) were investigated in macrophage (from Rab5a-/- and WT mice) following treatment with lipopolysaccharide or cecal ligation and puncture in vitro and in vivo, and in peripheral blood monocyte from sepsis patients and healthy volunteers. Results: We showed that propofol reduced membrane TLR4 expression on macrophage in vitro and in vivo. Rab5a participated in TLR4 intracellular trafficking and both Rab5a expression and the interaction between Rab5a and TLR4 were inhibited by propofol. We also showed Rab5a upregulation in peripheral blood monocyte of septic patients, accompanied by increased TLR4 expression on the cell surface. Both were correlated with SOFA score of sepsis patients and higher expression of Rab5a were found in septic non-survivors. Propofol downregulated the expression of Rab5a and TLR4 in these cells.Conclusions:We demonstrated that Rab5a regulates intracellular trafficking of TLR4 and that propofol reduces membrane TLR4 expression on macrophages by targeting Rab5a. Our study not only reveals a novel mechanism for the immunomodulatory effect of propofol but also indicates that Rab5a may be a potential therapeutic target against sepsis.


2008 ◽  
Vol 17 (3) ◽  
pp. 157-165 ◽  
Author(s):  
Niel C. Hoglen ◽  
Edward A. Abril ◽  
John-Michael Sauer ◽  
David L. Earnest ◽  
Robert S. McCuskey ◽  
...  

Diabetes ◽  
2012 ◽  
Vol 61 (5) ◽  
pp. 1281-1290 ◽  
Author(s):  
Katharine M. Irvine ◽  
Patricia Gallego ◽  
Xiaoyu An ◽  
Shannon E. Best ◽  
Gethin Thomas ◽  
...  

Blood ◽  
1999 ◽  
Vol 93 (1) ◽  
pp. 34-42 ◽  
Author(s):  
Katsuaki Sato ◽  
Hiroshi Kawasaki ◽  
Hitomi Nagayama ◽  
Ryo Serizawa ◽  
Junji Ikeda ◽  
...  

Abstract We examined the potential involvement of two CC chemokine receptors (CCRs), CCR-1 and CCR-3, in the functional activation of granulocyte-macrophage colony-stimulating factor (GM-CSF) plus interleukin-4 (IL-4)–generated human peripheral blood monocyte-derived immature dendritic cells (DCs). Flow cytometric analysis showed that CCR-1, CCR-3, CCR-5, and CXC chemokine receptor (CXCR)-4 were expressed on the cell surface of monocyte-derived DCs. Treatment with a monoclonal antibody (MoAb) to either CCR-1 or CCR-3 but not MoAbs to CCR-5 and CXCR-4 abolished chemotactic migration of monocyte-derived DCs. The DCs treated with either the anti–CCR-1 MoAb or anti–CCR-3 MoAb were less efficient than untreated DCs in proliferation of allogeneic T cells (TCs) and TC-derived secretion of interferon-γ (IFN-γ). The homotypic aggregation of DCs and heterotypic aggregation of DCs with TCs were suppressed by the anti–CCR-1 MoAb or anti–CCR-3 MoAb. These results indicate that CCR-1 and CCR-3 specifically regulate interaction of TCs and DCs in the process of antigen presentation.


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