scholarly journals Multipotent stromal cells skew monocytes towards an anti-inflammatory interleukin-10-producing phenotype by production of interleukin-6

Haematologica ◽  
2013 ◽  
Vol 98 (6) ◽  
pp. 888-895 ◽  
Author(s):  
S. M. Melief ◽  
S. B. Geutskens ◽  
W. E. Fibbe ◽  
H. Roelofs
Haematologica ◽  
2013 ◽  
Vol 98 (9) ◽  
pp. e121-e122 ◽  
Author(s):  
S. M. Melief ◽  
S. B. Geutskens ◽  
W. E. Fibbe ◽  
H. Roelofs

Haematologica ◽  
2013 ◽  
Vol 98 (9) ◽  
pp. e114-e114 ◽  
Author(s):  
D. Campioni ◽  
D. Bortolotti ◽  
O. R. Baricordi ◽  
R. Rizzo

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Nazli Jafarzadeh ◽  
Mohammad Ali Gholampour ◽  
Mohammad-Reza Alivand ◽  
Saeideh Kavousi ◽  
Laleh Arzi ◽  
...  

Abstract Background Leukemic cells facilitate the creation of the tumor-favorable microenvironment in the bone marrow niche using their secreted factors. There are not comprehensive details about immunosuppressive properties of chronic myelogenous leukemia-derived exosomes in the bone marrow stromal and immune compartment. We explained here that K562-derived exosomes could affect the gene expression, cytokine secretion, nitric oxide (NO) production, and redox potential of human primary cord blood-derived T cells (CB T cells). Methods Human primary cord blood-derived T cells were treated with K562-derived exosomes. We evaluated the expression variation of some critical genes activated in suppressor T cells. The alterations of some inflammatory and anti-inflammatory cytokines levels were assessed using ELISA assay and real-time PCR. Finally, NO production and intracellular ROS level in CB T cells were evaluated using Greiss assay and flow cytometry, respectively. Results Our results showed the over-expression of the genes involved in inhibitory T cells, including NQO1, PD1, and FoxP3. In contrast, genes involved in T cell activation such as CD3d and NFATc3 have been reduced significantly. Also, the expression of interleukin 10 (IL-10) and interleukin 6 (IL-6) mRNAs were significantly up-regulated in these cells upon exosome treatment. In addition, secretion of the interleukin 10, interleukin 6, and interleukin 17 (IL-17) proteins increased in T cells exposed to K562-derived exosomes. Finally, K562-derived exosomes induce significant changes in the NO production and intracellular ROS levels in CB T cells. Conclusions These results demonstrate that K562-derived exosomes stimulate the immunosuppressive properties in CB-derived T cells by inducing anti-inflammatory cytokines such as IL-10, reducting ROS levels, and arising of NO synthesis in these cells. Moreover, considering the elevation of FOXP3, IL-6, and IL-17 levels in these cells, exosomes secreted by CML cells may induce the fates of T cells toward tumor favorable T cells instead of conventional activated T cells.


2014 ◽  
Vol 66 (4) ◽  
pp. 1633-1640 ◽  
Author(s):  
Danijela Savic ◽  
Irena Lavrnja ◽  
Sanja Dacic ◽  
Ivana Bjelobaba ◽  
Nadezda Nedeljkovic ◽  
...  

Tiazofurin is a purine nucleoside analogue, with a broad spectrum of antitumoral and anti-inflammatory properties. In the present study, we have investigated the effect of tiazofurin on microglial inflammatory response to lipopolysaccharide in vitro. The cytotoxic effect of the drug was examined by sulforhodamine B assay. The Griess method was used to quantify nitrite production. Microglial morphology was assessed by measuring cell body size. Release of the pro-inflammatory cytokines, tumor necrosis factor-?, interleukin-1?, interleukin-6, and the anti-inflammatory cytokine interleukin- 10, were evaluated by enzyme-linked immunosorbent assay. Our data showed that tiazofurin decreased the number of activated microglia, lowered nitric oxide production and reduced the average cell surface of these cells. Tiazofurin reduced tumor necrosis factor-?, interleukin-6 and increased interleukin-10 secretion. Conversely, this drug promoted the release of interleukin-1?. Results obtained in this study indicate that TR displayed both anti- and pro-inflammatory modulation of activated microglia that could be relevant for its antitumor action within the central nervous system.


2022 ◽  
Author(s):  
GODSDAY UDOJI OGBUTOR ◽  
Eze Kingsley Nwangwa ◽  
Collins Ogbeivor ◽  
Nkemakonam Ezeonu ◽  
Ephraim Chukwuemeka ◽  
...  

Abstract BACKGROUND Chronic low grade systemic inflammation has been identified as a major risk factor for chronic diseases. The potential for physical exercise to induce anti-inflammatory effect is now increasingly being explored but there is paucity of data regarding the effects isometric exercise on inflammatory cytokines. The objective of this study was to investigate the responses of selected inflammatory cytokines to isometric handgrip exercise and identify possible effects of intensity and duration of the isometric effort on these variables. CASE PRESENTATION: A total of one hundred and ninety two (N=192) sedentary pre-hypertensive subjects, aged between 30-50years were recruited into the study and randomly distributed into three groups of 64 subjects each. The subjects performed a 24 consecutive day’s isometric hand grip exercise at 30% Maximum Voluntary Contraction. At the end of the 24 days, the group one (GP1) discontinued with the exercise protocol while the group two (GP2) continued the exercise protocol for another 24 consecutive days and the group three (GP3) continued with the exercise protocol for another 24 consecutive days but at 50%MVC. The parameters used to assess for the inflammatory cytokine variables included interleukin 10, interleukin 6 and tumor necrotic factor. At the end of the study, there was an increase in the resting values of interleukin 10 across the three groups while the resting values of interleukin 6 and tumor necrotic factor reduced significantly across groups. CONCLUSIONS: The reductions noted in the pro-inflammatory cytokines and increase in the anti-inflammatory cytokines could have a positive impact in the management of chronic diseases. It was also found that increase in intensity and/or duration produced more proportionate effect.


2009 ◽  
Vol 91 (5) ◽  
pp. 2185-2192 ◽  
Author(s):  
Yukiko Tagashira ◽  
Fuminori Taniguchi ◽  
Tasuku Harada ◽  
Ayako Ikeda ◽  
Ayako Watanabe ◽  
...  

Planta Medica ◽  
2018 ◽  
Vol 85 (04) ◽  
pp. 292-301 ◽  
Author(s):  
Jianqiang Zhang ◽  
Qian Zhang ◽  
Yangrong Xu ◽  
Huixiang Li ◽  
Fenglan Zhao ◽  
...  

AbstractGinseng is a perennial herb that contains various medicinal substances. The major active constituents of ginseng are ginsenosides, which have multifarious biological activities. Some pharmacological activities are closely dependent on the stereoisomers derived from the configuration at C20. In this study, the in vitro anti-inflammatory activity of C20 epimeric ocotillol-type triterpenes (2, 3, 9, and 10) and protopanaxadiol [20(S/R)-protopanaxadiol] were investigated. Epimers 2 and 3 were prepared starting from 20(S)-protopanaxadiol. Epimers 9 and 10 were synthesized from 20(R)-3-acetylprotopanaxadiol (7). The anti-inflammatory activity of 2, 3, 9, 10, 20(S)-protopanaxadiol, and 20(R)-protopanaxadiol was evaluated in cultured mouse macrophage RAW 264.7 cells. The MTT assay was used to measure the cytotoxicity. RAW 264.7 cells were stimulated by lipopolysaccharide to release the inflammatory mediators nitric oxide, prostaglandin E2, TNF-α, and interleukin-6 and anti-inflammatory mediator interleukin-10. The effect of the compounds on the overproduction of nitric oxide, prostaglandin E2, TNF-α, interleukin-6, and interleukin-10 was determined using Griess and ELISA methods. The results demonstrated that the in vitro anti-inflammatory activities of C20 epimeric ocotillol-type triterpenes and protopanaxadiol were different. Both the 20S-epimers (2 and 3) and 20R-epimers (9 and 10) inhibited the release of inflammatory mediator nitric oxide, while mainly the 20S-epimers inhibited the release of inflammatory mediator prostaglandin E2, and the 20R-epimers inhibited the release of inflammatory cytokine TNF-α. Both the 20S-epimers [2, 3, and 20(S)-protopanaxadiol] and 20R-epimers [9, 10, and 20(R)-protopanaxadiol] inhibited the release of inflammatory cytokine interleukin-6, but mainly the 20S-epimers [2, 3, and 20(S)-protopanaxadiol] increased the release of anti-inflammatory mediator interleukin-10.


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