Th17/Treg imbalance in patients with severe acute pancreatitis

Guo, JiGuang; Li, Zhen; Tang, Dan

doi:10.1097/md.0000000000021491

Cited by 14 publications

(23 citation statements)

References 32 publications

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“…The imbalance between Th17 cells and Tregs is common and relevant to the severity and prognosis of AP. Recent study confirmed that the proportion of Th17/Treg was significantly higher in SAP patients and more pronounced in the multiple organ failure group (P<0.05) (113). The homeostasis of the pancreatic microenvironment and rapid response to invaders are tightly regulated by the continuous adjustment between harmful Th17 cells and immunosuppressive Tregs, which establishes an ecological niche for bacterial intestinal border-dwelling bacteria (114).…”

Section: Microbiota-propelled T Helper 17 Cells In Apmentioning

confidence: 87%

“…Researchers found that continuous veno-venous hemofiltration (CVVH) removed IL-17 and other proinflammatory cytokines from serum, improved intestinal barrier function, and relieved systemic reactions. In addition, high-volume hemofiltration (HVHF) effectively attenuated the Th17/Treg imbalance during SAP ( 113 ). The Th17/Treg ratio and IL-17 were significantly reduced ( P <0.05) after HVHF, while no significant change was found in the non-HVHF group.…”

Section: Therapeutic Implications Of Apmentioning

confidence: 99%

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Role of Interleukin-17 in Acute Pancreatitis

Chen

Liu

et al. 2021

Front. Immunol.

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Acute pancreatitis (AP) is a leading cause of death and is commonly accompanied by systemic manifestations that are generally associated with a poor prognosis. Many cytokines contribute to pancreatic tissue damage and cause systemic injury. Interleukin-17 (IL-17) is a cytokine that may play a vital role in AP. Specifically, IL-17 has important effects on the immune response and causes interactions between different inflammatory mediators in the AP-related microenvironment. In this literature review, we will discuss the existing academic understanding of IL-17 and the impacts of IL-17 in different cells (especially in acinar cells and immune system cells) in AP pathogenesis. The clinical significance and potential mechanisms of IL-17 on AP deterioration are emphasized. The evidence suggests that inhibiting the IL-17 cytokine family could alleviate the pathogenic process of AP, and we highlight therapeutic strategies that directly or indirectly target IL-17 cytokines in acute pancreatitis.

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Section: Microbiota-propelled T Helper 17 Cells In Apmentioning

confidence: 87%

Section: Therapeutic Implications Of Apmentioning

confidence: 99%

Role of Interleukin-17 in Acute Pancreatitis

Chen

Liu

et al. 2021

Front. Immunol.

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“…It has been reported that dysregulation of immune responses may lead to the progression of AP (21,22). Guo et al (23) highlighted that the T helper 17 (Th17) cell/regulatory T cell (Treg) imbalance was involved in the development of AP and that it may be correlated with its severity and prognosis (24). Therefore, Treg cells play a key role in mediating the progression of AP.…”

Section: Emodin Inhibits the Progression Of Acute Pancreatitis Via Regulation Of Lncrna Tug1 And Exosomal Lncrna Tug1mentioning

confidence: 99%

Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1

Wen

Tang

et al. 2021

Mol Med Rep

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Acute pancreatitis (AP) is one of the most frequent gastrointestinal diseases and has no specific treatment. It has been shown that dysfunction of pancreatic acinar cells can lead to AP progression. Emodin is a natural product, which can alleviate the symptoms of AP. However, the mechanism by which emodin regulates the function of pancreatic acinar cells remains unclear. Thus, the present study aimed to investigate the mechanism by which emodin modulates the function of pancreatic acinar cells. To mimic AP in vitro, pancreatic acinar cells were cotreated with caerulein and lipopolysaccharide (LPS). Exosomes were isolated using the ExoQuick precipitation kit. Western blot analysis, Nanosight Tracking analysis and transmission electron microscopy were performed to detect the efficiency of exosome separation. Gene expression was detected by reverse transcription-quantitative PCR. The levels of IL-1β and TNF-α were detected by ELISA. The data indicated that emodin significantly decreased the levels of IL-1β and TNF-α in the supernatant samples derived from AR42J cells cotreated with caerulein and LPS. In addition, emodin significantly promoted the proliferation of AR42J cells cotreated with caerulein and LPS, and inhibited apoptosis, while the effect of emodin was reversed by long non-coding (lnc)RNA taurine upregulated 1 (TUG1) overexpression. The expression level of TUG1 in AR42J cells or exosomes derived from AR42J cells was significantly increased following treatment of the cells with LPS and caerulein, while this effect was notably reversed by emodin treatment. In addition, exosomes derived from caerulein and LPS cotreated AR42J cells inhibited the differentiation and anti-inflammatory function of regulatory T cells, while treatment of the cells with emodin significantly decreased this effect. In conclusion, the data indicated that emodin inhibited the induction of inflammation in AR42J cells by regulating the expression of cellular and exosomal lncRNA. Therefore, emodin may be used as a potential agent for the treatment of AP.

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“…The results suggested that the changes in cytokines could also be affected by other intestinal immune cells such as Peyer’s patches, which will be our future research direction. Tregs exert immunosuppressive effects by inhibiting INF-γ secretion and promoting IL-4, IL-10, and TGF-β secretion ( 64 , 65 ). A study has proved that Tregs were decreased and inversely associated with the serum concentration of TNF-α in SAP mice ( 66 ).…”

Section: Discussionmentioning

confidence: 99%

Dynamic Monitoring of Immunoinflammatory Response Identifies Immunoswitching Characteristics of Severe Acute Pancreatitis in Rats

et al. 2022

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BackgroundImmune dysfunction is the main characteristic of severe acute pancreatitis (SAP), and the timing of immune regulation has become a major challenge for SAP treatment. Previous reports about the time point at which the immune status of SAP changed from excessive inflammatory response to immunosuppression (hypo-inflammatory response) are conflicting.PurposesThe aims of this study are to explore the immunological dynamic changes in SAP rats from the perspective of intestinal mucosal immune function, and to determine the immunoswitching point from excessive inflammatory response to immunosuppression.MethodsRetrograde injection of sodium taurocholate into the pancreaticobiliary duct was applied to establish a SAP model in rats. The survival rate and the activities of serum amylase and pancreatic lipase in SAP rats were measured at different time points after model construction. The pathological changes in the pancreas and small intestines were analyzed, and the levels of intestinal pro- and anti-inflammatory cytokines and the numbers of intestinal macrophages, dendritic cells, Th1, Th2, and T regulatory cells were assessed. Meanwhile, the SAP rats were challenged with Pseudomonas aeruginosa (PA) strains to simulate a second hit, and the levels of intestinal inflammatory cytokines and the numbers of immune cells were analyzed to confirm the immunoswitching point.ResultsThe time periods of 12–24 h and 48–72 h were the two death peaks in SAP rats. The pancreas of SAP rats showed self-limiting pathological changes, and the switching period of intestinal cytokines, and innate and adaptive immunity indexes occurred at 24–48 h. It was further confirmed that 48 h after SAP model construction was the immunoswitching point from excessive inflammatory response to immunosuppression.ConclusionThe SAP rats showed characteristics of intestinal mucosal immune dysfunction after model construction, and the 48th h was identified as the immunoswitching point from excessive inflammatory response to immunosuppression. The results are of great significance for optimizing the timing of SAP immune regulation.

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Th17/Treg imbalance in patients with severe acute pancreatitis

Cited by 14 publications

References 32 publications

Role of Interleukin-17 in Acute Pancreatitis

Role of Interleukin-17 in Acute Pancreatitis

Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1

Dynamic Monitoring of Immunoinflammatory Response Identifies Immunoswitching Characteristics of Severe Acute Pancreatitis in Rats

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