Urinary Trypsin Inhibitor Attenuated Inflammatory Response of Patients Undergoing Cardiopulmonary Bypass by Inducing Activated Treg Cells

Hao, Xing; Han, Junyan; Xing, Zhichen; Yu, Honggang; Jiang, Chunjing; Zhang, Jianping; Yang, Jing; Hou, Xiaotong

doi:10.1007/s10753-013-9666-3

Cited by 8 publications

(10 citation statements)

References 20 publications

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“…Hence, inhibiting pro-inflammatory mediators [26, 27] and regulating immune reactions [25] are important considerations in the therapy of SAP. It has been confirmed that ulinastatin prevents the inflammatory response induced by SAP [28], and evidence also indicates that ulinastatin can regulate the immunological function through these special immune cells [18, 29]. In the present study, we demonstrated that in SAP rat model, pro-inflammatory cytokines TNF-α and IL-1β and anti-inflammatory cytokine IL-10 all were increased significantly, while TGF-β was decreased.…”

Section: Discussionsupporting

confidence: 75%

“…Another study indicated that ulinastatin can enhance immunological function and reduce the injury in SAP rats through inhibiting the apoptosis of CD4 + T cells [17]. Hao et al [18] showed that UTI can attenuate inflammatory response of patients undergoing cardiopulmonary bypass by inducing the expansion of CD4 + CD25 + Tregs. These studies suggested that CD4 + CD25 + Tregs may play important roles in preventing the inflammatory response of AP.…”

Section: Introductionmentioning

confidence: 99%

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Ulinastatin ameliorates tissue damage of severe acute pancreatitis through modulating regulatory T cells

et al. 2017

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BackgroundUlinastatin or urinary trypsin inhibitor (UTI) has been shown to ameliorate the inflammatory response induced by experimental severe acute pancreatitis (SAP) and hence reduce the mortality, however the mechanism of its action remains incompletely understood. We have investigated the effect of ulinastatin on regulatory T-cells (Tregs) in an established rat model of SAP.MethodsWe established a rat SAP model by injecting 5% Na-taurocholate into the pancreatic duct and treated the SAP rats with ulinastatin with different dose level (5000, 10000, 30000 U/kg) through intraperitoneal injection at 0, 6 and 12 h.ResultsWe showed that the tissue damage of pancreas and the mortality of the SAP rats were significantly reduced by ulinastatin. We also showed that in the SAP rats the frequencies of CD4+ T cells and Tregs, as well as the expressions of TGF-β1, CTLA-4, and Foxp3 were decreased in the SAP animals while IL-1β, IL-10 and TNF-α were significantly increased. Treatment with ulinastatin up-regulated the proportion of Tregs in CD4+ T cells and the expression of IL-10, Foxp3 and CTLA-4 in the SAP rats in a dose dependence fashion, while down-regulating the levels of L-1β and TNF-α, myeloperoxidase (MPO) activity.ConclusionsOur findings suggest that ulinastatin alleviates inflammatory response and tissue damage in SAP rats by increasing the proportion of Tregs. Our study provides a new mechanism for the beneficial effect of ulinastatin in SAP rat model.

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Section: Discussionsupporting

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Ulinastatin ameliorates tissue damage of severe acute pancreatitis through modulating regulatory T cells

et al. 2017

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“…Importantly, we demonstrated that immature CD14 low CD16 - monocytes contribute to the CPB-induced acute lung injury by generating their mature CD14 high CD16 + descendants, a major subset of cells producing TNF-α. At the same time, we observed that CPB induced an increase in the numbers of both rTreg and aTreg cells in patients undergoing cardiac surgery with CPB, 19 which supported the idea that CPB triggers compensatory inhibitory mechanisms to temper the inflammatory responses.…”

Section: Introductionsupporting

confidence: 74%

“…8,16,17 Human FoxP3 + CD4 + Treg cells comprise 3 phenotypically and functionally distinct subpopulations: resting Treg cells (rTreg cells) and activated Treg cells (aTreg cells), both of which have been shown to be suppressive in vitro, and cytokine-secreting non-Treg cells, which exhibit limited immunosuppressive activity, but are capable of producing IL-2, IL-17 and IFN-γ. 9,18,19…”

Section: Introductionmentioning

confidence: 99%

The effect of methylprednisolone prophylaxis on inflammatory monocyte subsets and suppressive regulatory T cells of patients undergoing cardiopulmonary bypass

et al. 2019

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Background: Cardiopulmonary bypass (CPB) during open-heart surgery triggers an inflammatory response that can cause significant morbidity and mortality. Human monocytes and regulatory T (Treg) cells are phenotypically and functionally heterogeneous and have been shown to play a significant role in the inflammatory dysfunction triggered by CPB. Glucocorticoids (GCs) have been widely administered for decades in patients undergoing CPB to reduce this inflammatory response. However, it has not been clearly established how routine prophylactic administration of glucocorticoids (GCs) affects monocyte and Treg subsets. Methods: Thirty-six patient who underwent heart surgery with CPB were randomly assigned to a methylprednisolone group (MG, N = 18; 500 mg in the CPB priming) and a non-methylprednisolone group (NMG, N = 18). The circulating monocyte and Treg subsets were analyzed by flow cytometry. Results: The MG and NMG groups had comparable percentages of monocyte subsets and similar expression levels of HLA-DR, CD86, CD64 and toll-like receptor 4 (TLR4). Remarkably, methylprednisolone increased the percentage of CD4+CD25+ Treg cells among CD4+ T cells in patients undergoing CPB, but did not increase the proportion of suppressive Treg cells, either resting or activated, in these patients undergoing CPB. Conclusions: Our results showed that prophylactic administration of methylprednisolone neither decreased the percentages and counts of inflammatory monocyte subsets nor did it induce the expansion of suppressive Treg cells in patients undergoing CPB. These results clarified the effects of GCs on cell-mediated immune responses and provided additional evidence in practice. Trial registration: Clinicaltrials.gov : NCT01296074. Registered 14 February 2011.

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“…Hence, inhibiting pro-inflammatory mediators [16,17] and regulating immune reactions are important considerations in the therapy of severe AP [15]. It has been confirmed that ulinastatin can regulate the immunological function through these special immune cells [18,19]. The pro-inflammatory cytokines such as IL-1β, IL-10, and TNF-α have been shown to play an important role in the pathogenesis of AP causing tissue damage and organ dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of anti-inflammatory drug ulinastatin in coronavirus disease 2019: A case report

Chatterjee¹,

Purayil²,

Ramakrishnan³

et al. 2020

IJCR

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Urinary Trypsin Inhibitor Attenuated Inflammatory Response of Patients Undergoing Cardiopulmonary Bypass by Inducing Activated Treg Cells

Cited by 8 publications

References 20 publications

Ulinastatin ameliorates tissue damage of severe acute pancreatitis through modulating regulatory T cells

Ulinastatin ameliorates tissue damage of severe acute pancreatitis through modulating regulatory T cells

The effect of methylprednisolone prophylaxis on inflammatory monocyte subsets and suppressive regulatory T cells of patients undergoing cardiopulmonary bypass

Efficacy of anti-inflammatory drug ulinastatin in coronavirus disease 2019: A case report

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