Eosinophils involved in fulminant hepatic failure are associated with high interleukin‐6 expression and absence of interleukin‐5 in liver and peripheral blood

Santos, Damião Carlos Moraes dos; Martinho, José Manoel; Pacheco-Moreira, L.F.; Araújo, Cristina Carvalho Viana de; Caroli-Bottino, Adriana; Pannain, Vera Lúcia; Trinta, Karen Soares; Gandini, Mariana; Neves, Patrícia Cristina da Costa; Matos, Denise Cristina de Souza; Caputo, Luzia Fátima Gonçalves; Pelajo-Machado, Marcelo; Pinto, Marcelo Alves

doi:10.1111/j.1478-3231.2008.01872.x

Cited by 14 publications

(6 citation statements)

References 41 publications

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“…Which was similar to the observations of fulminant hepatic failure where eosinophils with high IL-6 expression were reported to be involved in liver damage [41].…”

Section: Discussionsupporting

confidence: 91%

miRNA signatures can predict acute liver failure in hepatitis E infected pregnant females

Trehanpati

Sehgal

Patra

et al. 2017

Heliyon

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BackgroundAcute viral hepatitis E (AVH-E) can often result in acute liver failure (ALF) during pregnancy. microRNAs serve as mediators in drug induced liver failure. We investigated their role as a biomarker in predicting ALF due to HEV (ALF-E).MethodsWe performed next generation sequencing and subsequent validation studies in PBMCs of pregnant (P) self limiting AVH-E, ALF due to HEV (ALF-E) and compared with AVH-E in non-pregnant (NP) females and healthy controls.FindingsEleven microRNAs were significantly expressed in response to HEV infection; importantly, miR- 431, 654, 1468 and 4435, were distinctly expressed in pregnant self-limiting AVH-E and healthy females (p = 0.0005), but not in ALF-E. Sixteen exclusive microRNAs differentiated ALF-E from self limiting AVH-E in pregnant females. miR-450b which affects cellular proliferation and metabolic processes through RNF20 and SECB was predominanlty upregulated and correlated with poor outcome (ROC 0.958, p = 0.001).InterpretationOur results reveal that a specific microRNA profile can predict fatality in ALF-E in pregnancy. These microRNAs could be exploited as prognostic biomarkers and help in the development of new therapeutic interventions.

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“…Which was similar to the observations of fulminant hepatic failure where eosinophils with high IL-6 expression were reported to be involved in liver damage [41].…”

Section: Discussionsupporting

confidence: 91%

miRNA signatures can predict acute liver failure in hepatitis E infected pregnant females

Trehanpati

Sehgal

Patra

et al. 2017

Heliyon

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“…The elevated plasma levels of IL-8 that were detected in all cases of ALF are also described in patients with drug-induced ALF and are correlated with granulocyte migration into the liver parenchyma[5,41]. The elevated levels of circulating IL-6 and TNFα, also described by others[42,43], have been related to attempts at liver regeneration[44,45] and liver injury[46], respectively.…”

Section: Discussionmentioning

confidence: 92%

Changes in cellular proliferation and plasma products are associated with liver failure

Melgaço¹,

Soriani²,

Sucupira³

et al. 2016

WJH

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AIMTo study the differences in immune response and cytokine profile between acute liver failure and self-limited acute hepatitis.METHODSForty-six patients with self-limited acute hepatitis (AH), sixteen patients with acute liver failure (ALF), and twenty-two healthy subjects were involved in this study. The inflammatory and anti-inflammatory products in plasma samples were quantified using commercial enzyme-linked immunoassays and quantitative real-time PCR. The cellular immune responses were measured by proliferation assay using flow cytometry. The groups were divided into viral- and non-viral-induced self-limited AH and ALF. Thus, we worked with five groups: Hepatitis A virus (HAV)-induced self-limited acute hepatitis (HAV-AH), HAV-induced ALF (HAV-ALF), non-viral-induced self-limited acute hepatitis (non-viral AH), non-viral-induced acute liver failure (non-viral ALF), and healthy subjects (HC). Comparisons among HAV and non-viral-induced AH and ALF were performed.RESULTSThe levels of mitochondrial DNA (mtDNA) and the cytokines investigated [interleukin (IL)-6, IL-8, IL-10, interferon gamma, and tumor necrosis factor] were significantly increased in ALF patients, independently of etiology (P < 0.05). High plasma mtDNA and IL-10 were the best markers associated with ALF [mtDNA: OR = 320.5 (95%CI: 14.42-7123.33), P < 0.0001; and IL-10: OR = 18.8 (95%CI: 1.38-257.94), P = 0.028] and death [mtDNA: OR = 12.1 (95%CI: 2.57-57.07), P = 0.002; and IL-10: OR = 8.01 (95%CI: 1.26-50.97), P = 0.027]. In the cellular proliferation assay, NKbright, NKT and regulatory T cells (TReg) predominated in virus-specific stimulation in HAV-induced ALF patients with an anergic behavior in the cellular response to mitotic stimulation. Therefore, in non-viral-induced ALF, anergic behavior of activated T cells was not observed after mitotic stimulation, as expected and as described by the literature.CONCLUSIONmtDNA and IL-10 may be predictors of ALF and death. TReg cells are involved in immunological disturbance in HAV-induced ALF.

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“…C3 is a major component of the complement cascade, present at the early stage of liver inflammation [ 37 ], and C3 can regulate efflux and metabolism of steroid lipids in hepatocyte proliferation [ 18 , 38 ]. In our previous report, plasmatic elevation titers of systemic inflammatory mediators (TNF- α , IL-6, IL-8, IL-10, IFN γ , and total mtDNA) were demonstrated in ALF patients [ 7 , 22 , 23 , 39 ]. Similarly, other authors described the synergic effect of IL-1 beta and IL-6 on C3 mRNA transcription and C3 secretion in rat hepatocytes [ 40 ] since hepatocytes and Kupffer cells constitutively express receptors for C3 and C5a [ 40 , 41 ].…”

Section: Discussionmentioning

confidence: 98%

“…Inclusion criteria included the presence of coagulopathy (INR ≥ 1.5) and encephalopathy score above II, according to O'Grady et al [ 21 ] and as described previously [ 7 , 22 , 23 ]. Clinical details of the study population are shown in Table 1 .…”

Section: Methodsmentioning

confidence: 99%

Complement System as a Target for Therapies to Control Liver Regeneration/Damage in Acute Liver Failure Induced by Viral Hepatitis

Melgaço

Veloso

Pacheco-Moreira

et al. 2018

Journal of Immunology Research

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The complement system plays an important role in innate immunity inducing liver diseases as well as signaling immune cell activation in local inflammation regulating immunomodulatory effects such as liver damage and/or liver regeneration. Our aim is to evaluate the role of complement components in acute liver failure (ALF) caused by viral hepatitis, involving virus-induced ALF in human subjects using peripheral blood, samples of liver tissues, and ex vivo assays. Our findings displayed low levels of C3a in plasma samples with high frequency of C3a, C5a, and C5b/9 deposition in liver parenchyma. Meanwhile, laboratory assays using HepG2 (hepatocyte cell line) showed susceptibility to plasma samples from ALF patients impairing in vitro cell proliferation and an increase in apoptotic events submitting plasma samples to heat inactivation. In summary, our data suggest that the complement system may be involved in liver dysfunction in viral-induced acute liver failure cases using ex vivo assays. In extension to our findings, we provide insights into future studies using animal models for viral-induced ALF, as well as other associated soluble components, which need further investigation.

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Eosinophils involved in fulminant hepatic failure are associated with high interleukin‐6 expression and absence of interleukin‐5 in liver and peripheral blood

Cited by 14 publications

References 41 publications

miRNA signatures can predict acute liver failure in hepatitis E infected pregnant females

miRNA signatures can predict acute liver failure in hepatitis E infected pregnant females

Changes in cellular proliferation and plasma products are associated with liver failure

Complement System as a Target for Therapies to Control Liver Regeneration/Damage in Acute Liver Failure Induced by Viral Hepatitis

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