Differential early posttransplant cytokine responses in living and cadaver donor renal allografts

Sadeghi, Mahmoud; Daniel, Volker; Weimer, Rolf; Wiesel, M.; Hergesell, Olaf; Opelz, Gerhard

doi:10.1097/01.tp.0000063706.52369.ed

Cited by 14 publications

(10 citation statements)

References 28 publications

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“…Recently, we showed that DDKR mounted a stronger monocyte/macrophage response during the first two wk post‐transplant than LDKR. Conversely, the plasma level of sIL‐1RA early post‐transplant was significantly lower in DDKR than in LDKR (31). Based on the results of our previous and present studies, we believe that low production of sIL‐1RA in DDKT might contribute to severity of inflammation and a high incidence of DGF.…”

Section: Discussionmentioning

confidence: 93%

Decreasing plasma soluble IL‐1 receptor antagonist and increasing monocyte activation early post‐transplant may be involved in pathogenesis of delayed graft function in renal transplant recipients

Sadeghi¹,

Daniel²,

Naujokat³

et al. 2010

Clinical Transplantation

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Delayed graft function (DGF) increases the risk of acute allograft rejection and may affect long-term graft survival. We compared pre-transplant, early post-transplant, and late post-transplant serum creatinine (Cr) and plasma levels of neopterin, cytokines, and cytokine receptors/antagonists in patients with DGF (n = 39), slow graft function (SGF) (n = 43), or immediate graft function (IGF) (n = 30). Three and eight days post-transplant, plasma neopterin (p < 0.001; p < 0.001), Soluble Interleukin-6 (IL-6) receptor (R) (p = 0.002; p = 0.001), and IL-10 (p = 0.003; p = 0.001) were higher in DGF than IGF patients. One month post-transplant, plasma neopterin (p < 0.001) and IL-10 (p < 0.001) were higher in DGF than IGF patients. Three days post-transplant, the results indicated reduced sIL-1 receptor antognist (RA) production in DGF patients (p = 0.001). Simultaneously, plasma sIL-6R and IL-10 increased in DGF (p < 0.001; p = 0.003) and SGF (p = 0.007; p = 0.030) patients, indicating increased production of sIL-6R and IL-10. Lower sIL-1 production in DGF than IGF patients early post-transplant might promote the increased production of monocyte-derived neopterin, sIL-6R, and IL-10. This monocyte/macrophage activation might induce inflammation in the graft and subsequently cause an impairment of graft function. Blocking of monocyte activity after renal transplantation may be considered a potential approach for improving graft outcome.

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Section: Discussionmentioning

confidence: 93%

Decreasing plasma soluble IL‐1 receptor antagonist and increasing monocyte activation early post‐transplant may be involved in pathogenesis of delayed graft function in renal transplant recipients

Sadeghi¹,

Daniel²,

Naujokat³

et al. 2010

Clinical Transplantation

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“…This was confirmed through inhibition of IL-21 transcription in the presence of anti-IL-2, anti-IL-2R, and immunosuppressive agents. Therefore, it seems that IL-21 is crucial for the IL-2-dependent immune response [ 1 ]. Animal GVHD models have also confirmed the increased expression of IL-21 in male and female mice during the immune response.…”

Section: Discussionmentioning

confidence: 99%

“…Cytokines are key mediators of the immune response after transplantation [ 1 ]. Particular attention has been paid to the interleukin (IL)-2 cytokine family, which includes IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21, because of their importance in the allogenic response [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

IL2-IL21 gene cluster polymorphism is not associated with allograft function after kidney transplantation

et al. 2014

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Background Cytokines are key mediators of the immune response after transplantation. The interleukin (IL)-2 cytokine family, which includes IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21, is of particular interest because of its importance in the allogenic response. The aim of this study was to examine the association between the rs6822844 gene polymorphism in the IL2-IL21 region and allograft function after kidney transplantation.MethodsThe study enrolled 270 Caucasian kidney allograft recipients (166 males and 104 females, mean age 47.63 ± 12.96 years). Following parameters were recorded in each case: recipient’s age, delayed graft function (DGF), occurrence and number of episodes of acute rejection (AR), and chronic allograft dysfunction (CAD). Genotyping of the rs6822844 IL2-IL21 cluster gene polymorphism was performed using real-time PCR assay.ResultsThere were no statistically significant differences in the genotypes and alleles of the rs6822844 IL2-IL21 cluster gene polymorphism among patients with DGF (p = 0.72), AR (p = 0.69) and CAD (p = 0.77), or in creatinine concentrations 1, 3, 6, 12, 24 or 36 months after transplantation (p = 0.46, p = 0.58, p = 0.6, p = 0.72, p = 0.7, p = 0.76, respectively).ConclusionIt seems that the rs6822844 IL2-IL21 gene cluster polymorphism is of little importance in allograft function after kidney transplantation.

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“…Selectin blockade plus therapy with low-dose sirolimus and cyclosporine A prevented brain death-induced renal allograft dysfunction in rats (14). We showed previously that cadaver donor transplant recipients had a pro-inflammatory plasma cytokine response early posttransplant and developed more frequently ATN (15% vs. 9%) and delayed graft function (38% vs. 3%) than recipients of living donor transplants (15). Based on these observations it seemed conceivable to us that pretransplant activation of the recipient's immune system might accelerate and intensify the innate immune response against the graft and thereby contribute to the development of ATN.…”

mentioning

confidence: 89%

Association of High Pretransplant sIL-6R Plasma Levels with Acute Tubular Necrosis in Kidney Graft Recipients

et al. 2006

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Differential early posttransplant cytokine responses in living and cadaver donor renal allografts

Cited by 14 publications

References 28 publications

Decreasing plasma soluble IL‐1 receptor antagonist and increasing monocyte activation early post‐transplant may be involved in pathogenesis of delayed graft function in renal transplant recipients

Decreasing plasma soluble IL‐1 receptor antagonist and increasing monocyte activation early post‐transplant may be involved in pathogenesis of delayed graft function in renal transplant recipients

IL2-IL21 gene cluster polymorphism is not associated with allograft function after kidney transplantation

Association of High Pretransplant sIL-6R Plasma Levels with Acute Tubular Necrosis in Kidney Graft Recipients

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