Effects of Hypertonic Saline on CD4+CD25+Foxp3+ Regulatory T Cells After Hemorrhagic Shock in Relation to iNOS and Cytokines

Isayama, Kenji; Murao, Yoshinori; Saito, Fukuki; Hirakawa, Akihiko; Nakatani, Toshio

doi:10.1016/j.jss.2010.07.042

Cited by 13 publications

(11 citation statements)

References 29 publications

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“…Excessive activity or quantity of Tregs can promote infectious deterioration, sepsis, or tumor immune escape, whereas an insufficient amount can result in overactive inflammatory responses (Burgents et al, 2010;Fogle et al, 2010a;Carambia et al, 2014). Tregs have been shown to be differentially influenced by various resuscitation fluids after hemorrhagic shock (Murao et al, 2009;Isayama et al, 2012). In the present study, resuscitation with HTS did not alter the percentage of Tregs in the spleen, whereas NS and HES significantly lowered it.…”

Section: Discussioncontrasting

confidence: 42%

“…Recently, the immunologic effects of resuscitation with HTS solutions have been examined (Yip et al, 2007;Murao et al, 2009;Vincenzi et al, 2009;Isayama et al, 2012). HTS stimulates the rapid release of adenosine triphosphate (ATP) in a time-and concentrationdependent manner, which enhances T-cell activation by increasing Ca 2+ influx (Yip et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

“…HTS stimulates the rapid release of adenosine triphosphate (ATP) in a time-and concentrationdependent manner, which enhances T-cell activation by increasing Ca 2+ influx (Yip et al, 2007). In addition, HTS resuscitation suppresses the release of proinflammatory cytokines (Isayama et al, 2012), and thus might improve immunosuppressive reactions after hemorrhagic shock. Indeed, our previous studies indicate that HTS alleviates immune disorders and limits tissue injury after hemorrhagic shock (Lu et al, 2007;.…”

Section: Introductionmentioning

confidence: 99%

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Immune recovery after fluid resuscitation in rats with severe hemorrhagic shock

Feng

Jiang

et al. 2017

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To investigate the effects of resuscitation with normal saline (NS), hypertonic saline (HTS), and hydroxyethyl starch (HES) on regulatory T cells (Tregs), helper T 1 (Th1)/Th2 and cytotoxic T 1 (Tc1)/Tc2 profiles in the treatment of hemorrhagic shock. Methods: Rats subjected to severe hemorrhagic shock were resuscitated for 30 min with NS (n=8), HTS (n=8), or HES (n=8); sham (n=8) and naive control (n=8) groups were used for comparison. Following fluid resuscitation, the whole shed blood was reinfused for 30 min, and the rats were observed with continuous hemodynamic monitoring for 120 min. CD4 + CD25 + Foxp3 + Treg proportions, Th1/Th2 and Tc1/Tc2 profiles in spleen were analyzed by three-color flow cytometry. Results: The proportion of CD4 + CD25 + Foxp3 + Tregs and ratios of Th1/Th2 and Tc1/Tc2 did not differ among control, sham, and HTS groups, but were significantly lower in NS and HES groups (both P<0.05 vs. sham); NS and HES levels were similar. The level of Tc1 was significantly increased in HTS (P<0.05 vs. sham), and levels of Tc2 were increased in NS, HES, and HTS groups compared to sham (all P<0.05), but did not differ from each other. Conclusions: HTS resuscitation has a greater impact on immune system recovery than NS or HES by preserving the proportion of Tregs and maintaining the balance between Th1/Th2 and Tc1/Tc2 cells in the spleen. Thus, HTS resuscitation provides potential immunomodulatory activity in the early stage after hemorrhagic shock.

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Section: Discussioncontrasting

confidence: 42%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Immune recovery after fluid resuscitation in rats with severe hemorrhagic shock

Feng

Jiang

et al. 2017

J. Zhejiang Univ. Sci. B

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“…They generate large amounts of NO in the extrinsic environment, with a primary microbiocidal activity. iNOS can also be induced and expressed in virally-infected lymphocytes, specifically T cells, but little is known about its intrinsic effects in activated regulatory CD4+ T-cells [87][88][89][90][91].…”

Section: Expression Of Nitric Oxide Synthasesmentioning

confidence: 99%

Contribution of Inducible Nitric Oxide Synthase to the Transformation of HTLV-1 Infected CD4+ T-Cells

Baydoun¹,

Ratner²

2015

J Leuk

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The Human T-cell Leukemia Virus type 1 (HTLV-1), is the first retrovirus associated with a human cancer. HTLV-1 is the causative agent of an aggressive and fatal malignancy of CD4+ T lymphocytes known as Adult T-cell Leukemia lymphoma (ATLL). Since the discovery of the virus in 1980, intensive investigations have been undertaken to determine how HTLV-1 drives the transformation process in infected cells. This is because the oncogenic features of HTLV-1 make it an excellent tool to dissect the molecular pathways involved in cancer development. More important, HTLV-1 induced leukemia is a typical inflammation-mediated malignancy with constitutive activation of the NF-kB pathway, which is also a critical determinant in many other cancers. How NF-kB contributes to the leukemogenic process is not completely defined. We recently demonstrated that the NF-kB pathway induces the expression of inducible nitric oxide synthase (iNOS) in HTLV-1 induced leukemia. iNOS enzymatically generates nitric oxide, which is an oxidative and nitrosative agent of DNA and proteins. Nitric oxide was found to be associated with a large number of DNA Double Strand Breaks (DSBs) in HTLV-1 transformed cells. Here, we will review the major effects of nitric oxide on HTLV-1 induced leukemia.

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“…[7] Studies have shown that one mechanism of multiple organ damage is due to peroxynitrite, which is produced by the reaction of NO with reactive oxygen species that leads to nitrosative stress mediated organ injury. [78910]…”

Section: Introductionmentioning

confidence: 99%

Effects of aminoguanidine, a potent nitric oxide synthase inhibitor, on myocardial and organ structure in a rat model of hemorrhagic shock

Soliman

2014

J Emerg Trauma Shock

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Background:Nitric oxide (NO) has been shown to increase following hemorrhagic shock (HS). Peroxynitrite is produced by the reaction of NO with reactive oxygen species, leads to nitrosative stress mediated organ injury. We examined the protective effects of a potent inhibitor of NO synthase, aminoguanidine (AG), on myocardial and multiple organ structure in a rat model of HS.Materials and Methods:Male Sprague Dawley rats (300-350 g) were assigned to 3 experimental groups (n = 6 per group): (1) Normotensive rats (N), (2) HS rats and (3) HS rats treated with AG (HS-AG). Rats were hemorrhaged over 60 min to reach a mean arterial blood pressure of 40 mmHg. Rats were treated with 1 ml of 60 mg/kg AG intra-arterially after 60 min HS. Resuscitation was performed in vivo by the reinfusion of the shed blood for 30 min to restore normo-tension. Biopsy samples were taken for light and electron microscopy.Results:Histological examination of hemorrhagic shocked untreated rats revealed structural damage. Less histological damage was observed in multiple organs in AG-treated rats. AG-treatment decreased the number of inflammatory cells and mitochondrial swollen in myocardial cells.Conclusion:AG treatment reduced microscopic damage and injury in multiple organs in a HS model in rats.

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Effects of Hypertonic Saline on CD4+CD25+Foxp3+ Regulatory T Cells After Hemorrhagic Shock in Relation to iNOS and Cytokines

Cited by 13 publications

References 29 publications

Immune recovery after fluid resuscitation in rats with severe hemorrhagic shock

Immune recovery after fluid resuscitation in rats with severe hemorrhagic shock

Contribution of Inducible Nitric Oxide Synthase to the Transformation of HTLV-1 Infected CD4+ T-Cells

Effects of aminoguanidine, a potent nitric oxide synthase inhibitor, on myocardial and organ structure in a rat model of hemorrhagic shock

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