The Role of Interleukin-1β in Destruction of Transplanted Islets

Chen, Cheng; Rong, Pengfei; Yang, Min; Ma, Xiaoqian; Feng, Zhichao; Wang, Wei

doi:10.1177/0963689720934413

Cited by 10 publications

(12 citation statements)

References 109 publications

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“…IL-1β is one of the most important mediators of islet injury and plays an important role in the process of pancreatic islets dysfunction, which may represent an early inflammatory marker of graft failure ( 77 ). IL-1β is secreted by Kupffer cells, islet resident macrophages, and neutrophils around the transplantation site ( 78 ).…”

Section: Il-1βmentioning

confidence: 99%

“…IL-1β is secreted by Kupffer cells, islet resident macrophages, and neutrophils around the transplantation site ( 78 ). IL-1β secretion increases during islet acquisition, islet isolation, islet culture, and islet transplantation ( 77 ). IL-1β binds to the IL-1β receptor (IL-1βR) on the surface of pancreatic islet cells, causing TNF receptor-related factor 6 (TRAF6) to be activated by IL-1 receptor-related kinase (IRAK), which in turn leads to the phosphorylation and degradation of IκB.…”

Section: Il-1βmentioning

confidence: 99%

“…Then, in the process pancreas digestion and islet purification, enzymatic and mechanical stress can induce inflammatory mediators, such as IL-1β, in the islets ( 77 ). The islet basement membrane is lysed during the digestion and separation of the pancreas, which interrupts the communication between islet basement membrane proteins and the integrins expressed by the islets ( 83 ).…”

Section: Il-1βmentioning

confidence: 99%

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The Influence of Microenvironment on Survival of Intraportal Transplanted Islets

Yan

Chen

et al. 2022

Front. Immunol.

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Clinical islet transplantation has the potential to cure type 1 diabetes. Despite recent therapeutic success, it is still uncommon because transplanted islets are damaged by multiple challenges, including instant blood mediated inflammatory reaction (IBMIR), inflammatory cytokines, hypoxia/reperfusion injury, and immune rejection. The transplantation microenvironment plays a vital role especially in intraportal islet transplantation. The identification and targeting of pathways that function as “master regulators” during deleterious inflammatory events after transplantation, and the induction of immune tolerance, are necessary to improve the survival of transplanted islets. In this article, we attempt to provide an overview of the influence of microenvironment on the survival of transplanted islets, as well as possible therapeutic targets.

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Section: Il-1βmentioning

confidence: 99%

Section: Il-1βmentioning

confidence: 99%

Section: Il-1βmentioning

confidence: 99%

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The Influence of Microenvironment on Survival of Intraportal Transplanted Islets

Yan

Chen

et al. 2022

Front. Immunol.

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“…In this section, this review aims to briefly highlight findings from solid organ-specific fields regarding NLRP3 inflammasome involvement in either pre- or post-transplant pathology. Literature on NLRP3 inflammasome activation in the specific fields of hematopoietic stem cell transplant [ 87 , 88 , 89 ], pancreatic islet cell transplant [ 90 ], and post-transplant complications such as graft-versus-host disease and the development of myeloproliferative neoplasms [ 87 , 91 ] is abundant, and as such re-direction to the superlative existing recent review treatments of these fields is necessary.…”

Section: Nlrp3 Inflammasome Activation In End-stage Organ Failure and Transplantmentioning

confidence: 99%

The NLRP3 Inflammasome: Relevance in Solid Organ Transplantation

Burke

Dale

Dholakia

2021

IJMS

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The NOD, LRR, and pyrin domain-containing 3 (NLRP3) protein has been established as a central component of the inflammasome and regulates the inflammatory response to a myriad of environmental, microbial, and endogenous danger stimuli. Assembly of the NLRP3 inflammasome results in the cleavage and activation of caspase-1, in turn causing release of the pro-inflammatory interleukins 1-beta and 18. This activation response, while crucial to coordinated innate immune defense, can be aberrantly activated by the likes of cell-free DNA, and cause significant autoimmune pathology. Complications of autoimmunity induced by aberrant NLRP3 inflammasome activation have a great degree of mechanistic crossover with alloimmune injury in solid organ transplant, and stratagems to neutralize NLRP3 inflammasome activation may prove beneficial in solid organ transplant management. This article reviews NLRP3 inflammasome biology and the pathology associated with its hyperactivation, as well as the connections between NLRP3 inflammasome activation and allograft homeostasis.

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“…production (Chen et al, 2020a). The NO may interact with the DNA fragments and prosthetic groups in the transcription factor which resulting on the downregulated of glucose oxidation, oxygen consumption and ATP synthesis (Wang et al, 2010).…”

Section: ɛ and Pp Cellsmentioning

confidence: 99%

Recovery of isolated pancreatic isletsderived from gut leak-induced diabetes type ii mouse model

Soedarmanto¹

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Gut leak in the obese patient was known to be one of the predisposing factors causing diabetes type II. Indeed, the interleukin-10 (IL-10) plays a key role in gut mucosa homeostasis preventing the gut leak. Nevertheless, the linkage of diabetes type 2 caused by gut leak with IL-10 deficiency in the non-diabetes patient has not been investigated yet. Islets transplantation is known as the best alternative treatment for diabetes. The culture of isolated islets is still facing difficulties to preserve the morphology, viability, and functionality. Therefore, the present study was aiming to prove the concept of gut-leak on IL-10 deficient mice inducing diabetes type II and aiming to validate the way to preserve and recover the diabetes type II isolated islets using the newly established conditioned media. The 13-week-old age mice were separated into three groups (n=6/group) including background wildtype control (WT), transgenic control (IL-10KO), and gut leak-induced diabetes type II (GL-IL-10KO) which were induced by gavaging the dextran sulfate sodium (DSS). Then, mice were sacrificed, and the islets were isolated after 12 weeks nurtured and checked for morphology, viability, and functionality. The WT islets were used for validating two newly established conditioned media, VSCBIC-1 and VSCBIC-2, by using RPMI1640 as the basal and control medium. The GL-IL-10KO showed a defect in the viability and functionality of the isolated islets after isolation. Additionally, VSCBIC-1 was chosen as the best newly established conditioned media for preserving the WT isolated islets at least for 21 days. Then, VSCBIC-1 was used for culturing the GL-IL-10KO islets, and the results showed that the GL-IL-10KO could catch up the IL-10-KO and WT in term of viability. The functionality among GL-IL-10KO, IL-10-KO, and WT islets was upsurged gradually from day 0 to day 21. In brief, the GL-IL-10KO shows the defect on islets efficacy. Moreover, the newly established conditioned media VSCBIC-1 was able to recover the damaged islets in vitro.

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The Role of Interleukin-1β in Destruction of Transplanted Islets

Cited by 10 publications

References 109 publications

The Influence of Microenvironment on Survival of Intraportal Transplanted Islets

The Influence of Microenvironment on Survival of Intraportal Transplanted Islets

The NLRP3 Inflammasome: Relevance in Solid Organ Transplantation

Recovery of isolated pancreatic isletsderived from gut leak-induced diabetes type ii mouse model

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