Investigation of rhIL-10 inhibition of acute rejection after liver transplantation

Zou, X.M; Hirata, Koichi; Nie, G; Liang, Ying-Jian; Zhang, J.G; Qin, Hong; Zhang, B

doi:10.1016/s0041-1345(00)01598-0

Cited by 3 publications

(6 citation statements)

References 5 publications

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“…As for TNF‐α and IL‐1β, the role of IL‐10 may be different depending on the type and/or severity of I/R. Thus, the studies reported in the literature point to a beneficial effect of exogenous IL‐10 in nonsteatotic livers undergoing hepatic I/R9–12 and a minor role of endogenous IL‐10 in this process 38. However, our results suggest a beneficial role of both endogenous and exogenous IL‐10 on hepatic I/R injury, at least under the conditions evaluated in the present study.…”

Section: Discussioncontrasting

confidence: 46%

“…I/R + IL‐10 (n = 36): Same as group 2 but treated with recombinant rat IL‐10 (Peprotech EC Ltd.) at doses (i.v.) of 3 μg/kg (n = 12; 6 Ln and 6 Ob), 10 μg/kg (n = 12; 6 Ln and 6 Ob) and 30 μg/kg (n = 12; 6 Ln and 6 Ob), 5 minutes before ischemia 10, 11 PC + I/R + anti‐IL‐10 (n = 12): Same as group 3 but treated with anti‐IL‐10 at doses of 0.5 mg/kg (i.v.)…”

Section: Experimental Designmentioning

confidence: 99%

“…Interleukin‐1 (IL‐1) is primarily involved in promoting inflammatory processes, and blockade of IL‐1 action reduces tissue injury and mortality after hepatic I/R in nonsteatotic livers 5–8. In contrast, interleukin‐10 (IL‐10) show protective effects in nonsteatotic livers undergoing warm ischemia, and treatment with IL‐10 increased allograft survival in liver transplantation 9–12. Lipopolysaccharide (LPS) administration leads to similar IL‐1 levels in both normal and obese mice, whereas lower levels of IL‐10 and IL‐1 receptor antagonist (IL‐1ra) were detected after LPS induction in obese as compared to normal mice 13.…”

mentioning

confidence: 99%

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Ischemic preconditioning affects interleukin release in fatty livers of rats undergoing ischemia/reperfusion

et al. 2004

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Section: Discussioncontrasting

confidence: 46%

Section: Experimental Designmentioning

confidence: 99%

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confidence: 99%

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Ischemic preconditioning affects interleukin release in fatty livers of rats undergoing ischemia/reperfusion

et al. 2004

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“…iii. IL-10 is hepatoprotective and augments allograft survival following liver transplantation(22,(105)(106)(107). This quality has been confirmed for endogenous IL-10 in lean livers, but the effects of exogenous IL-10 depend on its dosage.…”

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confidence: 80%

Pathophysiological Changes During Ischemia-reperfusion Injury in Rodent Hepatic Steatosis

Neri

Dontas

Iliopoulos

et al. 2020

In Vivo

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Background/Aim: Ischemia and reperfusion injuries may produce deleterious effects on hepatic tissue after liver surgery and transplantation. The impact of ischemia-reperfusion injury (ΙRΙ) on the liver depends on its substrate, the percentage of liver ischemic tissue subjected to IRI and the ischemia time. The consequences of IRI are more evident in pathologic liver substrates, such as steatotic livers. This review is the result of an extended bibliographic PubMed search focused on the last 20 years. It highlights basic differences encountered during IRI in lean and steatotic livers based on studies using rodent experimental models. Conclusion: The main difference in cell death between lean and steatotic livers is the prevalence of apoptosis in the former and necrosis in the latter. There are also major changes in the effect of intracellular mediators, such as TNFα and IL-1β. Further experimental studies are needed in order to increase current knowledge of IRI effects and relevant mechanisms in both lean and steatotic livers, so that new preventive and therapeutic strategies maybe developed.

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“…Same as group 3, but the donors were treated with recombinant rat IL-10 (Peprotech EC Ltd., Rocky Hill, NJ) at doses of 10 µg/kg (i.v. ), just after BD was induced ( 15 , 40 , 41 ).…”

Section: Methodsmentioning

confidence: 99%

NO–IL-6/10–IL-1β axis: a new pathway in steatotic and non-steatotic liver grafts from brain-dead donor rats

Casillas-Ramírez,

Micó-Carnero,

Sánchez-González

et al. 2023

Front. Immunol.

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IntroductionBrain death (BD) and steatosis are both risk factors for organ dysfunction or failure in liver transplantation (LT)Material and methodsHere, we examine the role of interleukin 6 (IL- 6) and IL-10 in LT of both non-steatotic and steatotic liver recovered from donors after brain death (DBDs), as well as the molecular signaling pathways underlying the effects of such cytokines.ResultsBD reduced IL-6 levels only in nonsteatotic grafts, and diminished IL-10 levels only in steatotic ones. In both graft types, BD increased IL-1β, which was associated with hepatic inflammation and damage. IL-6 administration reduced IL-1β only in non-steatotic grafts and protected them against damage and inflammation. Concordantly, IL-1β inhibition via treatment with an IL-1 receptor antagonist caused the same benefits in non-steatotic grafts. Treatment with IL-10 decreased IL-1β only in steatotic grafts and reduced injury and inflammation specifically in this graft type. Blockading the IL-1β effects also reduced damage and inflammation in steatotic grafts. Also, blockade of IL-1β action diminished hepatic cAMP in both types of livers, and this was associated with a reduction in liver injury and inflammation, then pointing to IL-1β regulating cAMP generation under LT and BD conditions. Additionally, the involvement of nitric oxide (NO) in the effects of interleukins was evaluated. Pharmacological inhibition of NO in LT from DBDs prompted even more evident reductions of IL-6 or IL-10 in non-steatotic and steatotic grafts, respectively. This exacerbated the already high levels of IL-1β seen in LT from DBDs, causing worse damage and inflammation in both graft types. The administration of NO donors to non-steatotic grafts potentiated the beneficial effects of endogenous NO, since it increased IL-6 levels, and reduced IL-1β, inflammation, and damage. However, treatment with NO donors in steatotic grafts did not modify IL-10 or IL-1β levels, but induced more injurious effects tan the induction of BD alone, characterized by increased nitrotyrosine, lipid peroxidation, inflammation, and hepatic damage.ConclusionOur study thus highlights the specificity of new signaling pathways in LT from DBDs: NO–IL-6–IL-1β in non-steatotic livers and NO–IL-10–IL-1β in steatotic ones. This opens up new therapeutic targets that could be useful in clinical LT.

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Investigation of rhIL-10 inhibition of acute rejection after liver transplantation

Cited by 3 publications

References 5 publications

Ischemic preconditioning affects interleukin release in fatty livers of rats undergoing ischemia/reperfusion

Ischemic preconditioning affects interleukin release in fatty livers of rats undergoing ischemia/reperfusion

Pathophysiological Changes During Ischemia-reperfusion Injury in Rodent Hepatic Steatosis

NO–IL-6/10–IL-1β axis: a new pathway in steatotic and non-steatotic liver grafts from brain-dead donor rats

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