Effects of Hypertonic Saline and Hydroxyethyl Starch on Myeloid-Derived Suppressor Cells in Hemorrhagic Shock Mice under Secondary Bacterial Attack

Abstract

Objectives. The primary target is to reveal whether the resuscitation with hypertonic saline (HTS) or hydroxyethyl starch (HES) would have different effects on the myeloid-derived suppressor cell (MDSC) count and monocytic MDSC (M-MDSC)/granulocytic/neutrophilic MDSC (G-MDSC) rate in the peripheral blood, spleen, and bone marrow nucleated cells (BMNC) in a controlled hemorrhagic shock mouse model under secondary Escherichia coli bacterial infection attack, comparing to resuscitation with normal saline (NS) in 72 hours. Method. After hemorrhagic shock with bacteremia, which is induced by Escherichia coli 35218 injection, the mice were distributed into control, NS, HTS, and HES groups. The peripheral blood nucleated cells (PBNC), spleen single-cell suspension, and bone marrow nucleated cells were collected. The flow cytometry was used to detect the MDSC, M-MDSC, and G-MDSC. Result. In PBNC, after resuscitation with NS, the MDSC was continuously higher, while the rate of M-MDSC/G-MDSC were continuously lower (P<0.05). In HTS, the MDSC varied, higher at 24 and 72 hours (P<0.05), the M-MDSC/G-MDSC were continuously lower (P<0.05). In the spleen, resuscitation with HTS, the M-MDSC/G-MDSC were continuously lower (P<0.05). In BMNC, after resuscitation with HES, the M-MDSC/G-MDSC were lower at 24 and 72 hours (P<0.05). Conclusion. In mouse hemorrhagic shock model with bacterial infection, the resuscitation with NS, HTS, or HES induced difference changes in MDSC and M-MDSC/G-MDSC, which were time-dependent and organ-specific. Resuscitation with crystalloid, like NS or HTS, showed longer effects on the MDSC and M-MDSC/G-MDSC in peripheral blood; while HTS has a longer effect on M-MDSC/G-MDSC in the spleen, HES has a stronger impact on the differentiation regulation of MDSC to G-MDSC in the bone marrow.

Hydroxyethyl Starch Improves the Prognosis of Rats with Traumatic Shock via Activation of the ERK Signaling Pathway in Lymphocytes

“…Hydroxyethyl starch can “block” capillary leakage, effectively improve the hemorheological abnormalities of microcirculation, and increase tissue oxygen supply [ 4 ]. HES can significantly reduce the systemic inflammatory response and vascular endothelial injury after traumatic shock [ 5 ]. At the same time, it may induce the changes of lymphocyte proliferation and differentiation by destroying the balance of proinflammatory response and anti-inflammatory response marked by the level of serum IL-2, IL-4, γ -IFN, etc.…”

Xiaoliu Pingyi Recipe Inhibits Lung Pre-Metastatic Niche Formation and Prevents Myeloid-Derived Suppressor Cells Recruitment

“…G-MDSCs and M-MDSCs were identified as CD11b + Ly6G + Ly6C − , and CD11b + Ly6G − Ly6C + cells, respectively. 20 , 21 …”

“…G-MDSCs and M-MDSCs were identified as CD11b + Ly6G + Ly6C − , and CD11b + Ly6G − Ly6C + cells, respectively. 20,21 Western Blotting Analysis On day 14 after tumor implantation, lung tissues were collected, homogenized, and lysed in RIPA buffer to extract total protein. Protein concentration was measured using a BCA protein assay kit (P0012, Beyotime).…”

Characteristics of New Oxygen-Carrying Plasma and Its Application Prospects in the Treatment of Severe Acute Pancreatitis

“…After ischemia, the intestinal tract releases pro-inflammatory molecules, such as superoxide anion free radicals and cytokines, causing the intestinal flora to shift and enter the portal vein and systemic circulatory system, leading to intestinal remote organ failure. 41,42 A study has shown that HES-130 infusion inhibits the release of pro-inflammatory cytokines, such as tumor necrosis factor α and interleukin 6, 43 which may be the reason for the improvement in intestinal barrier dysfunction. [44][45][46] Our new type of oxygen-carrying plasma can be used for the treatment of severe acute pancreatitis through the mechanism of HES by improving intestinal oxygen metabolism, reducing the release of inflammatory mediators, and protecting the integrity of the intestinal barrier.…”