Tumour necrosis factor-α plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients

Dalboni, Maria Aparecida; Quinto, Beata Marie Redublo; Grabulosa, Caren Cristina; Narciso, Roberto Camargo; Monte, Julio Cesar Martins; Durão, Marcelino S.; Rizzo, Luiz Vicente; Cendoroglo, Miguel; Santos, OF Pavão dos; Batista, Marcelo Costa

doi:10.1111/cei.12100

Cited by 17 publications

(33 citation statements)

References 30 publications

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“…In the rat severe burn model, the mRNA level of TNF-α, IL-1β and ICAM-1 in renal tissue was increased significantly. On the contrary, the level of IL-10, an anti-inflammatory cytokine3940, was significantly suppressed in the kidney of severely burned rats and recovered after the administration of melatonin. Based on the results we deduced that melatonin could attenuate the inflammatory response through inhibiting the expression of pro-inflammatory cytokines and up-regulating the expression of anti-inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 95%

Melatonin prevents acute kidney injury in severely burned rats via the activation of SIRT1

Bai

Gao

et al. 2016

Sci Rep

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Acute kidney injury (AKI) is a common complication after severe burns. Melatonin has been reported to protect against multiple organ injuries by increasing the expression of SIRT1, a silent information regulator that regulates stress responses, inflammation, cellular senescence and apoptosis. This study aimed to investigate the protective effects of melatonin on renal tissues of burned rats and the role of SIRT1 involving the effects. Rat severely burned model was established, with or without the administration of melatonin and SIRT1 inhibitor. The renal function and histological manifestations were determined to evaluate the severity of kidney injury. The levels of acetylated-p53 (Ac-p53), acetylated-p65 (Ac-p65), NF-κB, acetylated-forkhead box O1 (Ac-FoxO1), Bcl-2 and Bax were analyzed to study the underlying mechanisms. Our results suggested that severe burns could induce acute kidney injury, which could be partially reversed by melatonin. Melatonin attenuated oxidative stress, inflammation and apoptosis accompanied by the increased expression of SIRT1. The protective effects of melatonin were abrogated by the inhibition of SIRT1. In conclusion, we demonstrate that melatonin improves severe burn-induced AKI via the activation of SIRT1 signaling.

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Section: Discussionmentioning

confidence: 95%

Melatonin prevents acute kidney injury in severely burned rats via the activation of SIRT1

Bai

Gao

et al. 2016

Sci Rep

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“…Secreted by immunocytes, TNF-α, IL-1β and IL-6 are involved in the activation of macrophages, lymphocytes and cytotoxic cells; leukocyte/endothelial adhesion; and the induction of acute-phase protein[ 1 ]. In particular, IL-10 is a negative-regulator cytokine generated by immunocytes that antagonises the inflammatory response and regulates autoimmune activity [ 39 ]. The tissue level of IL-10 is usually elevated as an intrinsic anti-inflammatory system responding to exogenous stimuli.…”

Section: Discussionmentioning

confidence: 99%

Beneficial Effects of Hydrogen-Rich Saline on Early Burn-Wound Progression in Rats

et al. 2015

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IntroductionDeep burn wounds undergo a dynamic process known as wound progression that results in a deepening and extension of the initial burn area. The zone of stasis is more likely to develop more severe during wound progression in the presence of hypoperfusion. Hydrogen has been reported to alleviate injury triggered by ischaemia/reperfusion and burns in various organs by selectively quenching oxygen free radicals. The aim of this study was to investigate the possible protective effects of hydrogen against early burn-wound progression.MethodsDeep-burn models were established through contact with a boiled, rectangular, brass comb for 20 s. Fifty-six Sprague-Dawley rats were randomly divided into sham, burn plus saline, and burn plus hydrogen-rich saline (HS) groups with sacrifice and analysis at various time windows (6 h, 24 h, 48 h) post burn. Indexes of oxidative stress, apoptosis and autophagy were measured in each group. The zone of stasis was evaluated using immunofluorescence staining, ELISA, and Western blot to explore the underlying effects and mechanisms post burn.ResultsThe burn-induced increase in malondialdehyde was markedly reduced with HS, while the activities of endogenous antioxidant enzymes were significantly increased. Moreover, HS treatment attenuated increases in apoptosis and autophagy postburn in wounds, according to the TUNEL staining results and the expression analysis of Bax, Bcl-2, caspase-3, Beclin-1 and Atg-5 proteins. Additionally, HS lowered the level of myeloperoxidase and expression of TNF-α, IL-1β, and IL-6 in the zone of stasis while augmenting IL-10. The elevated levels of Akt phosphorylation and NF-κB p65 expression post burn were also downregulated by HS management.ConclusionHydrogen can attenuate early wound progression following deep burn injury. The beneficial effect of hydrogen was mediated by attenuating oxidative stress, which inhibited apoptosis and inflammation, and the Akt/NF-κB signalling pathway may be involved in regulating the release of inflammatory cytokines.

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“…Furthermore, the low-producing genotypes of the aforementioned polymorphisms were associated with the risk of AKI, as were the haplotypes T-C-A of TNFA and C-A-C-G of IL-10 . Dalboni et al [ 41 ] showed that the GG genotype of TNFA − 308 polymorphism and AA genotype of IL-10 –1082 polymorphism, when combined, are associated with AKI and/or death, and also with RRT and/or death. Susantitaphong et al [ 30 ] found that TNFA gene −308 G/A A-allele was associated with higher peak serum creatinine and urinary kidney injury molecule-1 (KIM-1), as well as higher multi organ failure (MOF) score in hospitalized patients with AKI.…”

Section: Resultsmentioning

confidence: 99%

“…Typically, associations found with such an approach have been difficult to replicate and the coverage of genetic variation has been poor [ 51 ]. Regardless of some reported positive associations [ 22 , 24 , 25 , 27 – 35 , 38 , 40 , 41 , 44 – 50 ], no conclusive data on predisposing genetic variants exist.…”

Section: Discussionmentioning

confidence: 99%

“…First, the balance between pro- and anti-inflammatory mediators was among the most investigated. Polymorphism rs1800629 in the TNFA gene is suspected to alter the inflammatory response and to be associated with AKI susceptibility [ 41 , 45 ], as well as outcome [ 27 , 30 , 41 ]. This finding is controversial, however; in five studies [ 25 , 36 , 40 , 42 , 44 ] no evidence supported an association between TNFA and susceptibility or outcome of AKI.…”

Section: Discussionmentioning

confidence: 99%

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Genetic predisposition to acute kidney injury – a systematic review

2015

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BackgroundThe risk of an individual to develop an acute kidney injury (AKI), or its severity, cannot be reliably predicted by common clinical risk factors. Whether genetic risk factors have an explanatory role poses an interesting question, however. Thus, we conducted a systematic literature review regarding genetic predisposition to AKI or outcome of AKI patients.MethodsWe searched Ovid SP (MEDLINE) and EMBASE databases and found 4027 references to AKI. Based on titles and abstracts, we approved 37 articles for further analysis. Nine were published only as abstracts, leaving 28 original articles in the final analysis. We extracted the first author, year of publication, study design, clinical setting, number of studied patients, patients with AKI, ethnicity of patients, studied polymorphisms, endpoints, AKI definition, phenotype, significant findings, and data for quality scoring from each article. We summarized the findings and scored the quality of articles.ResultsThe articles were quite heterogeneous and of moderate quality (mean 6.4 of 10).ConclusionsDespite different gene polymorphisms with suggested associations with development or severity or outcome of AKI, definitive conclusions would require replication of associations in independent cohort studies and, preferably a hypothesis-free study design.Electronic supplementary materialThe online version of this article (doi:10.1186/s12882-015-0190-6) contains supplementary material, which is available to authorized users.

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Tumour necrosis factor-α plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients

Cited by 17 publications

References 30 publications

Melatonin prevents acute kidney injury in severely burned rats via the activation of SIRT1

Melatonin prevents acute kidney injury in severely burned rats via the activation of SIRT1

Beneficial Effects of Hydrogen-Rich Saline on Early Burn-Wound Progression in Rats

Genetic predisposition to acute kidney injury – a systematic review

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