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CLC number: R605.971

On-line Access: 2017-01-03

Received: 2016-11-10

Revision Accepted: 2016-12-13

Crosschecked: 2016-12-16

Cited: 0

Clicked: 1578

Citations:  Bibtex RefMan EndNote GB/T7714

 ORCID:

Yuan-qiang Lu

http://orcid.org/0000-0002-9057-4344

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Journal of Zhejiang University SCIENCE B 2017 Vol.18 No.1 P.48-58

http://doi.org/10.1631/jzus.B1600510


Distribution and differentiation of myeloid-derived suppressor cells after fluid resuscitation in mice with hemorrhagic shock


Author(s):  Jiu-kun Jiang, Wen Fang, Liang-jie Hong, Yuan-qiang Lu

Affiliation(s):  Department of Emergency Medicine, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China; more

Corresponding email(s):   luyuanqiang@zju.edu.cn

Key Words:  Hemorrhagic shock, Hydroxyethyl starch, Hypertonic saline, Myeloid-derived suppressor cells, Normal saline


Jiu-kun Jiang, Wen Fang, Liang-jie Hong, Yuan-qiang Lu. Distribution and differentiation of myeloid-derived suppressor cells after fluid resuscitation in mice with hemorrhagic shock[J]. Journal of Zhejiang University Science B, 2017, 18(1): 48-58.

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author="Jiu-kun Jiang, Wen Fang, Liang-jie Hong, Yuan-qiang Lu",
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publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1600510"
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%T Distribution and differentiation of myeloid-derived suppressor cells after fluid resuscitation in mice with hemorrhagic shock
%A Jiu-kun Jiang
%A Wen Fang
%A Liang-jie Hong
%A Yuan-qiang Lu
%J Journal of Zhejiang University SCIENCE B
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%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1600510

TY - JOUR
T1 - Distribution and differentiation of myeloid-derived suppressor cells after fluid resuscitation in mice with hemorrhagic shock
A1 - Jiu-kun Jiang
A1 - Wen Fang
A1 - Liang-jie Hong
A1 - Yuan-qiang Lu
J0 - Journal of Zhejiang University Science B
VL - 18
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EP - 58
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PB - Zhejiang University Press & Springer
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DOI - 10.1631/jzus.B1600510


Abstract: 
Objective: To investigate the distribution and differentiation of myeloid-derived suppressor cells (MDSCs) in hemorrhagic shock mice, which are resuscitated with normal saline (NS), hypertonic saline (HTS), and hydroxyethyl starch (HES). Methods: BALB/c mice were randomly divided into control, NS, HTS, and HES resuscitation groups. Three subgroups (n=8) in each resuscitation group were marked as 2, 24, and 72 h. Flow cytometry was used to detect the MDSCs, monocytic MDSCs (M-MDSCs), and granulocytic/neutrophilic MDSCs (G-MDSCs) in peripheral blood nucleated cells (PBNCs), spleen single-cell suspension, and bone marrow nucleated cells (BMNCs). Results: The MDSCs in BMNCs among three resuscitation groups were lower 2 h after shock, in PBNCs of the HTS group were higher, and in spleen of the NS group were lower (all P<0.05 vs. control). The M-MDSC/G-MDSC ratios in PBNCs of the HTS and HES groups were lower (both P<0.05 vs. control). At 24 h, the MDSCs in PBNCs of the NS and HTS groups were higher, while the spleen MDSCs in the HTS group were higher (all P<0.05 vs. control). The M-MDSC/ G-MDSC ratios were all less in PBNCs, spleen, and BMNCs of the NS and HTS groups, and were lower in BMNCs of the HES group (all P<0.05 vs. control). At 72 h, the elevated MDSCs in PBNCs were presented in the HTS and HES groups, and in spleen the augment turned up in three resuscitation groups (all P<0.05 vs. control). The inclined ratios to M-MDSC were exhibited in spleen of the NS and HTS groups, and in PBNCs of the NS group; the inclination to G-MDSC in BMNCs was shown in the HES group (all P<0.05 vs. control). Conclusions: HTS induces the earlier elevation of MDSCs in peripheral blood and spleen, and influences its distribution and differentiation, while HES has a less effect on the distribution but a stronger impact on the differentiation of MDSCs, especially in bone marrow.

失血性休克小鼠液体复苏后髓源性抑制细胞的分布和分化

目的:在失血性休克小鼠模型中使用不同的液体复苏,包括等渗盐水(NS)、高渗盐水(HTS)和羟乙基淀粉(HES),比较在不同时间点髓源性抑制细胞(MDSCs)在外周血、脾脏和骨髓组织中分布和分化的情况。
创新点:(1)创建失血性休克小鼠模型;(2)将MDSCs引入失血性休克液体复苏后免疫变化的研究中;(3)对骨髓、脾脏和外周血细胞中的MDSCs分布进行研究,并探讨了在失血性休克不同液体复苏后MDSCs的分化趋势,为临床上形成规范的救治方案提供了科学的实践资料。
方法:将BALB/c雄性小鼠随机分成四组,除对照组外,其余三组在建立失血性休克小鼠模型后采用不同的液体复苏:NS组、HTS组和HES组。在模型建立后的2、24和72 h分批次处死小鼠,取外周血、脾脏和骨髓细胞组织,通过三色荧光标记流式细胞术进一步分析MDSC细胞含量,以及其两亚组单核髓源性抑制细胞(M-MDSC)和中性粒髓源性抑制细胞(G-MDSC)的比值。
结论:HTS可诱导MDSCs在外周血和脾脏中的早期积累,并影响MDSCs分化和分布;而HES对MDSCs的分布影响较小,但对MDSCs在骨髓中的分化影响较大。

关键词:失血性休克;羟乙基淀粉;高渗盐水;髓源性抑制细胞;等渗盐水

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

[1]Anna, B., Massimo, C., Simone, G., et al., 2016. Pilot randomized controlled trial evaluating the effect of hypertonic saline with and without hyaluronic acid in reducing inflammation in cystic fibrosis. J. Aerosol. Med. Pulm. Drug Deliv., 29(6):482-489.

[2]Arun, S., Burawat, J., Sukhorum, W., et al., 2016. Changes of testicular phosphorylated proteins in response to restraint stress in male rats. J. Zhejiang Univ.-Sci. B (Biomed. & Biotechnol.), 17(1):21-29.

[3]Brudecki, L., Ferguson, D.A., McCall, C.E., et al., 2012. Myeloid-derived suppressor cells evolve during sepsis and can enhance or attenuate the systemic inflammatory response. Infect. Immun., 80(6):2026-2034.

[4]Bulger, E.M., Jurkovich, G.J., Nathens, A.B., et al., 2008. Hypertonic resuscitation of hypovolemic shock after blunt trauma: a randomized controlled trial. Arch. Surg., 143(2):139-148, discussion 149.

[5]Bulger, E.M., May, S., Kerby, J.D., et al., 2011. Out-of-hospital hypertonic resuscitation after traumatic hypovolemic shock: a randomized, placebo controlled trial. Ann. Surg., 253(3):431-441.

[6]Chang, M., Tang, H., Liu, D., et al., 2016. Comparison of melatonin, hypertonic saline, and hydroxyethyl starch for resuscitation of secondary intra-abdominal hypertension in an animal model. PLoS ONE, 11(8):e0161688.

[7]Chen, G., You, G., Wang, Y., et al., 2013. Effects of synthetic colloids on oxidative stress and inflammatory response in hemorrhagic shock: comparison of hydroxyethyl starch 130/0.4, hydroxyethyl starch 200/0.5, and succinylated gelatin. Crit. Care, 17(4):R141.

[8]Chen, L.W., Su, M.T., Chen, P.H., et al., 2011. Hypertonic saline enhances host defense and reduces apoptosis in burn mice by increasing Toll-like receptors. Shock, 35(1):59-66.

[9]Choi, S.H., Yoon, Y.H., Kim, J.Y., et al., 2014. The effect of hypertonic saline on mRNA of proinflammatory cytokines in lipopolysaccharide-stimulated polymorphonuclear cells. Curr. Ther. Res., 76:58-62.

[10]Coimbra, R., Junger, W.G., Hoyt, D.B., et al., 1996. Hypertonic saline resuscitation restores hemorrhage-induced immunosuppression by decreasing prostaglandin E2 and interleukin-4 production. J. Surg. Res., 64(2):203-209.

[11]Cuenca, A.G., Delano, M.J., Kelly-Scumpia, K.M., et al., 2011. A paradoxical role for myeloid-derived suppressor cells in sepsis and trauma. Mol. Med., 17(3-4):281-292.

[12]Delano, M.J., Scumpia, P.O., Weinstein, J.S., et al., 2007. MyD88-dependent expansion of an immature GR-1+CD11b+ population induces T cell suppression and Th2 polarization in sepsis. J. Exp. Med., 204(6):1463-1474.

[13]Dong, F., Chen, W., Xu, L., et al., 2014. Therapeutic effects of compound hypertonic saline on rats with sepsis. Braz. J. Infect. Dis., 18(5):518-525.

[14]Duan, C., Li, T., Liu, L., 2015. Efficacy of limited fluid resuscitation in patients with hemorrhagic shock: a meta-analysis. Int. J. Clin. Exp. Med., 8(7):11645-11656.

[15]Dufait, I., Schwarze, J.K., Liechtenstein, T., et al., 2015. Ex vivo generation of myeloid-derived suppressor cells that model the tumor immunosuppressive environment in colorectal cancer. Oncotarget, 6(14):12369-12382.

[16]Esnault, P., Prunet, B., Cotte, J., et al., 2013. Hydroxyethyl starch 130/0.4 or hypertonic saline solution to decrease inflammatory response in hemorrhagic shock? Crit. Care, 17(5):457.

[17]Gamboni, F., Anderson, C., Sanchayita, M., et al., 2016. Hypertonic saline primes activation of the p53‒p21 signaling axis in human small airway epithelial cells that prevents inflammation induced by pro-inflammatory cytokines. J. Proteome Res., 15(10):3813-3826.

[18]Heim, C.E., Vidlak, D., Scherr, T.D., et al., 2014. Myeloid-derived suppressor cells contribute to Staphylococcus aureus orthopedic biofilm infection. J. Immunol., 192(8):3778-3792.

[19]Huang, H., Liu, J., Hao, H., et al., 2016. G-CSF administration after the intraosseous infusion of hypertonic hydroxyethyl starches accelerating wound healing combined with hemorrhagic shock. BioMed Res. Int., 2016:5317630.

[20]Huang, L.Q., Zhu, G.F., Deng, Y.Y., et al., 2014. Hypertonic saline alleviates cerebral edema by inhibiting microglia-derived TNF-α and IL-1β-induced Na-K-Cl Cotransporter up-regulation. J. Neuroinflammation, 11:102.

[21]Huber-Lang, M., Gebhard, F., Schmidt, C.Q., et al., 2016. Complement therapeutic strategies in trauma, hemorrhagic shock and systemic inflammation—closing Pandora’s box? Semin. Immunol., 28(3):278-284.

[22]Igarashi, T., Fujimoto, C., Suzuki, H., et al., 2014. Short-time exposure of hyperosmolarity triggers interleukin-6 expression in corneal epithelial cells. Cornea, 33(12):1342-1347.

[23]Janols, H., Bergenfelz, C., Allaoui, R., et al., 2014. A high frequency of MDSCs in sepsis patients, with the granulocytic subtype dominating in gram-positive cases. J. Leukoc. Biol., 96(5):685-693.

[24]Junger, W.G., Rhind, S.G., Rizoli, S.B., et al., 2012. Resuscitation of traumatic hemorrhagic shock patients with hypertonic saline—without dextran—inhibits neutrophil and endothelial cell activation. Shock, 38(4):341-350.

[25]Ke, Q.H., Zheng, S.S., Liang, T.B., et al., 2006. Pretreatment of hypertonic saline can increase endogenous interleukin 10 release to attenuate hepatic ischemia reperfusion injury. Dig. Dis. Sci., 51(12):2257-2263.

[26]Lai, D., Qin, C., Shu, Q., 2014. Myeloid-derived suppressor cells in sepsis. BioMed Res. Int., 2014:598654.

[27]Liu, H., Xiao, X., Sun, C., et al., 2015. Systemic inflammation and multiple organ injury in traumatic hemorrhagic shock. Front. Biosci., 20:927-933.

[28]Liu, Z., Li, Y., Liu, B., et al., 2013. Synergistic effects of hypertonic saline and valproic acid in a lethal rat two-hit model. J. Trauma Acute Care Surg., 74(4):991-998.

[29]Loomis, W.H., Namiki, S., Hoyt, D.B., et al., 2001. Hypertonicity rescues T cells from suppression by trauma-induced anti-inflammatory mediators. Am. J. Physiol. Cell Physiol., 281(3):C840-C848.

[30]Lu, Y.Q., Huang, W.D., Cai, X.J., et al., 2008. Hypertonic saline resuscitation reduces apoptosis of intestinal mucosa in a rat model of hemorrhagic shock. J. Zhejiang Univ.-Sci. B, 9(11):879-884.

[31]Lu, Y.Q., Gu, L.H., Huang, W.D., et al., 2010. Effect of hypertonic saline resuscitation on heme oxygenase-1 mRNA expression and apoptosis of the intestinal mucosa in a rat model of hemorrhagic shock. Chin. Med. J. (Engl.), 123(11):1453-1458.

[32]Lu, Y.Q., Gu, L.H., Zhang, Q., et al., 2013. Hypertonic saline resuscitation contributes to early accumulation of circulating myeloid-derived suppressor cells in a rat model of hemorrhagic shock. Chin. Med. J. (Engl.), 126(7):1317-1322.

[33]Makarenkova, V.P., Bansal, V., Matta, B.M., et al., 2006. CD11b+/Gr-1+ myeloid suppressor cells cause T cell dysfunction after traumatic stress. J. Immunol., 176(4):2085-2094.

[34]Motaharinia, J., Etezadi, F., Moghaddas, A., et al., 2015. Immunomodulatory effect of hypertonic saline in hemorrhagic shock. DARU J. Pharm. Sci., 23:47.

[35]Nagaraj, S., Youn, J.I., Gabrilovich, D.I., 2013. Reciprocal relationship between myeloid-derived suppressor cells and T cells. J. Immunol., 191(1):17-23.

[36]Naumann, D.N., Beaven, A., Dretzke, J., et al., 2016. Searching for the optimal fluid to restore microcirculatory flow dynamics after haemorrhagic shock: a systematic review of preclinical studies. Shock, 46(6):609-622.

[37]O'Connor, M.A., Fu, W.W., Green, K.A., et al., 2015. Subpopulations of M-MDSCs from mice infected by an immunodeficiency-causing retrovirus and their differential suppression of T- vs B-cell responses. Virology, 485:263-273.

[38]Ost, M., Singh, A., Peschel, A., et al., 2016. Myeloid-derived suppressor cells in bacterial infections. Front. Cell Infect. Microbiol., 6:37.

[39]Öztürk, T., Onur, E., Cerrahoğlu, M., et al., 2015. Immune and inflammatory role of hydroxyethyl starch 130/0.4 and fluid gelatin in patients undergoing coronary surgery. Cytokine, 74(1):69-75.

[40]Wang, P., Li, Y., Li, J., 2009. Protective roles of hydroxyethyl starch 130/0.4 in intestinal inflammatory response and oxidative stress after hemorrhagic shock and resuscitation in rats. Inflammation, 32(2):71-82.

[41]Watters, J.M., Tieu, B.H., Todd, S.R., et al., 2006. Fluid resuscitation increases inflammatory gene transcription after traumatic injury. J. Trauma, 61(2):300-309.

[42]Wright, F.L., Gamboni, F., Moore, E.E., et al., 2014. Hyperosmolarity invokes distinct anti-inflammatory mechanisms in pulmonary epithelial cells: evidence from signaling and transcription layers. PLoS ONE, 9(12):e114129.

[43]Youn, J.I., Nagaraj, S., Collazo, M., et al., 2008. Subsets of myeloid-derived suppressor cells in tumor-bearing mice. J. Immunol., 181(8):5791-5802.

[44]Youn, J.I., Kumar, V., Collazo, M., et al., 2013. Epigenetic silencing of retinoblastoma gene regulates pathologic differentiation of myeloid cells in cancer. Nat. Immunol., 14(3):211-220.

[45]Zhang, Q., Lu, Y.Q., Jiang, J.K., et al., 2012. Early changes of CD4+CD25+Foxp3+ regulatory T cells and Th1/Th2, Tc1/Tc2 profiles in the peripheral blood of rats with controlled hemorrhagic shock and no fluid resuscitation. Chin. Med. J. (Engl.), 125(12):2163-2167.

[46]Zhou, J., Donatelli, S.S., Gilvary, D.L., et al., 2016. Therapeutic targeting of myeloid-derived suppressor cells involves a novel mechanism mediated by clusterin. Sci. Rep., 6:29521.

[47]Zoglmeier, C., Bauer, H., Nörenberg, D., et al., 2011. CpG blocks immunosuppression by myeloid-derived suppressor cells in tumor-bearing mice. Clin. Cancer Res., 17(7):1765-1775.

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