Interleukin 18 (IL-18) upregulation in acute rejection of kidney allograft

Striz, Ilja; Krasna, Eliska; Honsová, Eva; Lácha, J; Petříčková, Kateřina; Jaresova, Marcela; Lodererová, Alena; Böhmová, Radka; Valhova, Sarka; Slavčev, Antonij; Vı́tko, Štefan

doi:10.1016/j.imlet.2005.01.010

Cited by 73 publications

(41 citation statements)

References 25 publications

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“…These profiles correlated with the progression of allograft rejection and their gene products were therefore suggested to be the main modulators of the anti-alloantigen response. Importantly, these factors have also been implicated in solid organ allograft rejection [28–35]. The development of a full-scale anti-alloantigenic response was apparent from the infiltration of immune cells into the entire allograft at POD 5, while the cell infiltrate in POD 5 syngrafts remained confined to the graft-recipient, as typically observed in wound healing responses.…”

Section: Discussionmentioning

confidence: 99%

Immunological and inflammatory mapping of vascularized composite allograft rejection processes in a rat model

et al. 2017

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BackgroundHand and face vascularized composite allotransplantation (VCA) is an evolving and challenging field with great opportunities. During VCA, massive surgical damage is inflicted on both donor and recipient tissues, which may contribute to the high VCA rejection rates. To segregate between the damage-induced and rejection phase of post-VCA responses, we compared responses occurring up to 5 days following syngeneic versus allogeneic vascularized groin flap transplantations, culminating in transplant acceptance or rejection, respectively.MethodsThe immune response elicited upon transplantation of a syngeneic versus allogeneic vascularized groin flap was compared at Post-operative days 2 or 5 by histology, immunohistochemistry and by broad-scope gene and protein analyses using quantitative real-time PCR and Multiplex respectively.ResultsImmune cell infiltration began at the donor-recipient interface and paralleled expression of a large group of wound healing-associated genes in both allografts and syngrafts. By day 5 post-transplantation, cell infiltration spread over the entire allograft but remained confined to the wound site in the syngraft. This shift correlated with upregulation of IL-18, INFg, CXCL9, 10 and 11, CCL2, CCL5, CX3CL1 and IL-10 in the allograft only, suggesting their role in the induction of the anti-alloantigen adaptive immune response.ConclusionsHigh resemblance between the cues governing VCA and solid organ rejection was observed. Despite this high resemblance we describe also, for the first time, a damage induced inflammatory component in VCA rejection as immune cell infiltration into the graft initiated at the surgical damage site spreading to the entire allograft only at late stage rejection. We speculate that the highly inflammatory setting created by the unique surgical damage during VCA may enhance acute allograft rejection.

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Section: Discussionmentioning

confidence: 99%

Immunological and inflammatory mapping of vascularized composite allograft rejection processes in a rat model

et al. 2017

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“…Immunohistochemical staining of protocol biopsies showed constitutive IL-18 expression in the epithelium of distal tubules with the induction of immunoreactivity in acute rejection patients where also proximal tubules, infiltrating leukocytes, and endothelium were strongly positive. Furthermore, serum levels of IL-18 were significantly elevated in patients with acute rejection of kidney allograft as compared to patients with uncomplicated outcome of kidney transplantation and subjects with acute tubulointerstitial nephropathy [93]. …”

Section: Interleukin-18 (Il-18)mentioning

confidence: 99%

New Biomarkers for the Quick Detection of Acute Kidney Injury

2013

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Acute kidney injury (AKI) is a common and strong problem in the diagnosis of which based on measurement of BUN and serum creatinine. These traditional methods are not sensitive and specific for the diagnosis of AKI. AKI is associated with increased morbidity and mortality in critically ill patients and a quick detection is impossible with BUN and serum creatinine. A number of serum and urinary proteins have been identified that may messenger AKI prior to a rise in BUN and serum creatinine. New biomarkers of AKI, including NGAL, KIM-1, cystatin-C, IL-18, and L-FABP, are more favourable tests than creatinine which have been identified and studied in several experimental and clinical training. This paper will discuss some of these new biomarkers and their potential as useful signs of AKI. We searched the literature using PubMed and MEDLINE with acute kidney injury, urine, and serum new biomarkers and the articles were selected only from publication types in English.

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“…The source of IL-18 was postulated to be from MCs and/or infiltrating leukocytes. Moderate levels of IL-18 expression have also been detected in MCs and podocytes from biopsies of acute renal allograft rejection [25]. Our results show that amongst intrinsic glomerular cells, only MCs significantly increased IL-18 production after LPS stimulation, suggesting that MCs, apart from infiltrating leukocytes, may be a major source of IL-18 within the glomerulus during the pathogenesis of glomerular diseases.…”

Section: Discussionmentioning

confidence: 51%

Stimulation of Mesangial Cells by Angiotensin II and Lipopolysaccharide Increases Expression of Interleukin-18, but Not IL-18 Receptor

Hardy

Hambly²,

Ko³

et al. 2010

Nephron Exp Nephrol

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Background/Aims: Mesangial cell (MC) hyperplasia is associated with several kidney diseases. Experimental studies confirm upregulation of IL-18 in glomerular disease and renal allograft rejection. We evaluated whether MCs express IL-18 and IL-18 receptor-α (IL-18Rα) with and without stimulation by LPS, AngII and PDGF. Methods: Glomeruli were isolated using Dynabeads perfusion. MCs were cultured by glomerular explantation. IL-18 and IL-18Rα expression were detected by RT-PCR, ELISA and flow cytometry. Results: Significantly higher levels of IL-18 expression were detected in isolated glomeruli, compared to cortical tissue devoid of glomeruli, and in MCs, compared to tubular cells (both p < 0.01). Increased IL-18 expression was detected in MCs, but not podocytes, endothelial cells or tubular cells in response to LPS stimulation. IL-18 mRNA and protein expression were significantly upregulated by AngII (p < 0.05) and LPS (p < 0.01), but not PDGF-BB, in primary MCs and a MC line (MES13). IL-18Rα mRNA was almost undetectable in MCs treated with or without LPS, AngII and PDGF-BB. IL-18Rα protein was not detected by flow cytometry. Conclusions: MCs express IL-18, which was significantly increased after LPS and AngII stimulation, but do not express appreciable levels of IL-18Rα. MC-derived IL-18 is unlikely to be an autocrine mediator in glomerular disease given the lack of IL-18Rα.

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Interleukin 18 (IL-18) upregulation in acute rejection of kidney allograft

Cited by 73 publications

References 25 publications

Immunological and inflammatory mapping of vascularized composite allograft rejection processes in a rat model

Immunological and inflammatory mapping of vascularized composite allograft rejection processes in a rat model

New Biomarkers for the Quick Detection of Acute Kidney Injury

Stimulation of Mesangial Cells by Angiotensin II and Lipopolysaccharide Increases Expression of Interleukin-18, but Not IL-18 Receptor

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