Ischemia Reperfusion Injury Triggers CXCL13 Release and B-Cell Recruitment After Allogenic Kidney Transplantation

Kreimann, Kirill; Jang, Mi-Sun; Rong, Song; Greite, Robert; Vietinghoff, Sibylle von; Schmitt, Roland; Bräsen, Jan Hinrich; Schiffer, Lena; Gerstenberg, Jessica; Vijayan, Vijith; Dittrich–Breiholz, Oliver; Wang, Li; Karsten, Christian M.; Gwinner, Wilfried; Haller, Hermann; Immenschuh, Stephan; Gueler, Faikah

doi:10.3389/fimmu.2020.01204

Cited by 21 publications

(12 citation statements)

References 36 publications

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“…After reperfusion, the microvascular injury caused by ischemia enhances fluid filtration, with leukocyte plugging in capillaries and damaged endothelial cells secreting factors to favor inflammatory mediators and proteolytic enzymes ( 146 ). The global outcome of this ischemia-reperfusion damage is a harmful environment that through DAMPS and PAMPS enhances both innate and cellular immunity ( 147 ).…”

Section: The Harmsmentioning

confidence: 99%

Chronic Kidney Allograft Disease: New Concepts and Opportunities

et al. 2021

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Chronic kidney disease (CKD) is increasing in most countries and kidney transplantation is the best option for those patients requiring renal replacement therapy. Therefore, there is a significant number of patients living with a functioning kidney allograft. However, progressive kidney allograft functional deterioration remains unchanged despite of major advances in the field. After the first post-transplant year, it has been estimated that this chronic allograft damage may cause a 5% graft loss per year. Most studies focused on mechanisms of kidney graft damage, especially on ischemia-reperfusion injury, alloimmunity, nephrotoxicity, infection and disease recurrence. Thus, therapeutic interventions focus on those modifiable factors associated with chronic kidney allograft disease (CKaD). There are strategies to reduce ischemia-reperfusion injury, to improve the immunologic risk stratification and monitoring, to reduce calcineurin-inhibitor exposure and to identify recurrence of primary renal disease early. On the other hand, control of risk factors for chronic disease progression are particularly relevant as kidney transplantation is inherently associated with renal mass reduction. However, despite progress in pathophysiology and interventions, clinical advances in terms of long-term kidney allograft survival have been subtle. New approaches are needed and probably a holistic view can help. Chronic kidney allograft deterioration is probably the consequence of damage from various etiologies but can be attenuated by kidney repair mechanisms. Thus, besides immunological and other mechanisms of damage, the intrinsic repair kidney graft capacity should be considered to generate new hypothesis and potential therapeutic targets. In this review, the critical risk factors that define CKaD will be discussed but also how the renal mechanisms of regeneration could contribute to a change chronic kidney allograft disease paradigm.

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Section: The Harmsmentioning

confidence: 99%

Chronic Kidney Allograft Disease: New Concepts and Opportunities

et al. 2021

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“…Additionally, renal grafts inevitably experience ischemia as soon as they are removed from the donor. IRI is a well-known risk factor for the development of delayed graft function [ 22 , 23 ]. Although most renal graft transplant recipients can completely recover from the initial period, clinical evidence has demonstrated that transplanted kidneys with prolonged ischemic periods are more susceptible to long-term deterioration [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Amelioration of Renal Injury by Resveratrol in a Rat Renal Transplantation Model via Activation of the SIRT1/NF-κB Signaling Pathway

Zhou

Xiang

et al. 2022

BioMed Research International

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Purpose. The improvement of the long-term survival of patients receiving kidney transplantation remains challenging. Ischemia reperfusion injury (IRI) reduces long-term renal graft survival in the early posttransplantation phase. However, few studies have investigated the effects of IRI on the pathogenesis of chronic renal graft failure. Silent information regulator 1 (SIRT1) regulates antioxidative stress and inflammatory response and protects against IRI. This study is aimed at investigating the role of resveratrol (RSV), an SIRT1 activator, in preventing renal injury in a rat renal transplantation model. Methods. A classical F334-to-LEW orthotopic renal transplantation rat model was established. The experiment group was treated with RSV from three days prior to kidney transplantation and the treatment lasted until the day of harvest. Uninephrectomized F344 and Lewis rats were used as controls. After 12 weeks, the effects of RSV were evaluated according to renal function, histopathology, immunohistochemistry, and western blotting. The activities of oxidative stress-related markers and proinflammatory cytokines were also assessed. Results. RSV treatment significantly ameliorated renal function and histopathological lesions in kidney-transplanted rats and increased the levels of GSH, SOD, and CAT and decreased the levels of MDA and iNOS. Furthermore, RSV also inhibited the expression of proinflammatory cytokines/chemokines such as TNF-α, CD68, and IL-6 in kidney-transplanted rats. In addition, the transplant group displayed significantly lower level of SIRT1 and higher level of Ac-NF-κBp65. RSV increased the expression of SIRT1 and decreased the expression of Ac-NF-κBp65. Conclusion. SIRT1 plays an important role in the pathogenesis of chronic renal allograft dysfunction. It is a potential therapeutic agent for ameliorating inflammation and oxidative stress-induced renal injury following kidney transplantation by activating the SIRT1/NF-κB signaling pathway.

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“…We found that the infiltration levels of activated B cells and immature B cells were higher in the high CPC score group, suggesting a potential connection between the level of B-cell infiltration and the outcome in patients with CA. Previously, the study by Kreimann et al showed that ischemia/reperfusion injury after allogeneic renal transplantation triggers CXCL13 release and B-cell recruitment [ 41 ]. In addition, the study by Renner et al showed that B-cell subsets contribute to renal injury and renal protection after ischemia/reperfusion.…”

Section: Discussionmentioning

confidence: 99%

Identification and Validation of Novel Potential Pathogenesis and Biomarkers to Predict the Neurological Outcome after Cardiac Arrest

Zhang

Liu

et al. 2022

Brain Sciences

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Predicting neurological outcomes after cardiac arrest remains a major issue. This study aimed to identify novel biomarkers capable of predicting neurological prognosis after cardiac arrest. Expression profiles of GSE29540 and GSE92696 were downloaded from the Gene Expression Omnibus (GEO) database to obtain differentially expressed genes (DEGs) between high and low brain performance category (CPC) scoring subgroups. Weighted gene co-expression network analysis (WGCNA) was used to screen key gene modules and crossover genes in these datasets. The protein-protein interaction (PPI) network of crossover genes was constructed from the STRING database. Based on the PPI network, the most important hub genes were identified by the cytoHubba plugin of Cytoscape software. Eight hub genes (RPL27, EEF1B2, PFDN5, RBX1, PSMD14, HINT1, SNRPD2, and RPL26) were finally screened and validated, which were downregulated in the group with poor neurological prognosis. In addition, GSEA identified critical pathways associated with these genes. Finally, a Pearson correlation analysis showed that the mRNA expression of hub genes EEF1B2, PSMD14, RPFDN5, RBX1, and SNRPD2 were significantly and positively correlated with NDS scores in rats. Our work could provide comprehensive insights into understanding pathogenesis and potential new biomarkers for predicting neurological outcomes after cardiac arrest.

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Ischemia Reperfusion Injury Triggers CXCL13 Release and B-Cell Recruitment After Allogenic Kidney Transplantation

Cited by 21 publications

References 36 publications

Chronic Kidney Allograft Disease: New Concepts and Opportunities

Chronic Kidney Allograft Disease: New Concepts and Opportunities

Amelioration of Renal Injury by Resveratrol in a Rat Renal Transplantation Model via Activation of the SIRT1/NF-κB Signaling Pathway

Identification and Validation of Novel Potential Pathogenesis and Biomarkers to Predict the Neurological Outcome after Cardiac Arrest

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