The role of macrophages in the development of biliary injury in a lipopolysaccharide-aggravated hepatic ischaemia-reperfusion model

Reiling, Janske; Bridle, Kim R.; Schaap, Frank G.; Jaskowski, L.; Santrampurwala, Nishreen; Britton, L.; Campbell, Catherine; Jansen, Petér L. M.; Damink, Steven W. M. Olde; Crawford, Darrell H. G.; Dejong, C.H.C.; Fawcett, Jonathan

doi:10.1016/j.bbadis.2017.06.028

Cited by 4 publications

(4 citation statements)

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“…LPS-induced hepatic injury is the pathological basis of varied hepatic diseases. However, the injury is considered indirect and induced by the production of pro-inflammatory cytokines from activated Kupffer cells[ 12 ]. In this current study, we found that serum levels of AST and ALT were visibly high in both β-arrestin 2 KO and WT mice treated with LPS for 4 h (Figure 1A and B).…”

Section: Discussionmentioning

confidence: 99%

β-arrestin 2 attenuates lipopolysaccharide-induced liver injuryviainhibition of TLR4/NF-κB signaling pathway-mediated inflammation in mice

Jiang¹,

Xu²,

Guo³

et al. 2018

WJG

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AIMTo study the role and the possible mechanism of β-arrestin 2 in lipopolysaccharide (LPS)-induced liver injury in vivo and in vitro.METHODSMale β-arrestin 2+/+ and β-arrestin 2-/- C57BL/6J mice were used for in vivo experiments, and the mouse macrophage cell line RAW264.7 was used for in vitro experiments. The animal model was established via intraperitoneal injection of LPS or physiological sodium chloride solution. Blood samples and liver tissues were collected to analyze liver injury and levels of pro-inflammatory cytokines. Cultured cell extracts were collected to analyze the production of pro-inflammatory cytokines and expression of key molecules involved in the TLR4/NF-κB signaling pathway.RESULTSCompared with wild-type mice, the β-arrestin 2 knockout mice displayed more severe LPS-induced liver injury and significantly higher levels of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and IL-10. Compared with the control group, pro-inflammatory cytokines (including IL-1β, IL-6, TNF-α, and IL-10) produced by RAW264.7 cells in the β-arrestin 2 siRNA group were significantly increased at 6 h after treatment with LPS. Further, key molecules involved in the TLR4/NF-κB signaling pathway, including phospho-IκBα and phosho-p65, were upregulated.CONCLUSIONβ-arrestin 2 can protect liver tissue from LPS-induced injury via inhibition of TLR4/NF-κB signaling pathway-mediated inflammation.

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Section: Discussionmentioning

confidence: 99%

β-arrestin 2 attenuates lipopolysaccharide-induced liver injuryviainhibition of TLR4/NF-κB signaling pathway-mediated inflammation in mice

Jiang¹,

Xu²,

Guo³

et al. 2018

WJG

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“…To directly explore the role of periphery macrophages in the pathogenesis of PD, we depleted the macrophages by intraperitoneally injecting clodronate liposomes, which has been used in several stress and LPS studies (Kotter et al, 2001 ; Zhu et al, 2015 ; Reiling et al, 2018 ). We used the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced mouse model of PD to assess the activation status of macrophages in peripheral immune system.…”

Section: Introductionmentioning

confidence: 99%

Partial Depletion of Peripheral M1 Macrophages Reverses Motor Deficits in MPTP-Treated Mouse by Suppressing Neuroinflammation and Dopaminergic Neurodegeneration

Yan

Zhang

Lin

et al. 2018

Front. Aging Neurosci.

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Background: Neuroinflammation plays an important role in the pathogenesis of Parkinson's disease (PD). Inflammatory cytokines in the peripheral immune system can induce neuroinflammation in central nervous system (CNS). Whether the peripheral immune system is involved in PD is unclear. The present study investigated the contribution of the peripheral immune system to the neuronal loss in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) model of PD.Methods: MPTP was intraperitoneally injected into mice to generate a PD model. Mice received clodronate liposomes every 3 days to deplete peripheral macrophages. The percentages of macrophages were measured by flow cytometry at 1, 3, and 7 days after MPTP injection. Neurobehavioral parameters, protein expression, inflammatory cytokines release, and microglia activation were measured by the open field test, western blotting, quantitative polymerase chain reaction (qPCR), and immunofluorescence staining, respectively at 7 days after MPTP injection.Results: Our study revealed that intraperitoneal injection of MPTP could increase peripheral M1 macrophages levels. It also can induce T cells infiltration and cytokine release. Depletion of M1 macrophages by clodronate liposomes suppressed these inflammatory effects and blunted the loss of TH+ nigral neurons and functional impairments caused by MPTP.Conclusion: Our results indicated the critical role of M1 macrophages in the pathogenesis of PD and proposed inhibition of M1 macrophages as a promising therapeutic approach for neurodegeneration.

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“…Moreover, when the ischemic myocardium recovers blood flow, due to the production of oxygen free radicals, the damaged cardiomyocytes release endogenous risk signals to recruit inflammatory cells to nest, start/amplify local inflammatory response, resulting in secondary damage of cardiomyocytes [51] . Inhibition of excessive inflammatory response can reduce the area of myocardial infarction and improve cardiac function [52] , [53] . It is confirmed that the local changes of I/R injury are mainly inflammatory reaction with neutrophil and monocyte infiltration [11] , [51] .…”

Section: Discussionmentioning

confidence: 99%

Iminostilbene, a novel small-molecule modulator of PKM2, suppresses macrophage inflammation in myocardial ischemia–reperfusion injury

Tian

Luo

et al. 2021

Journal of Advanced Research

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The role of macrophages in the development of biliary injury in a lipopolysaccharide-aggravated hepatic ischaemia-reperfusion model

Cited by 4 publications

References 38 publications

β-arrestin 2 attenuates lipopolysaccharide-induced liver injuryviainhibition of TLR4/NF-κB signaling pathway-mediated inflammation in mice

β-arrestin 2 attenuates lipopolysaccharide-induced liver injuryviainhibition of TLR4/NF-κB signaling pathway-mediated inflammation in mice

Partial Depletion of Peripheral M1 Macrophages Reverses Motor Deficits in MPTP-Treated Mouse by Suppressing Neuroinflammation and Dopaminergic Neurodegeneration

Iminostilbene, a novel small-molecule modulator of PKM2, suppresses macrophage inflammation in myocardial ischemia–reperfusion injury

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