M1- and M2-macrophage polarization in rat liver cirrhosis induced by thioacetamide (TAA), focusing on Iba1 and galectin-3

Wijesundera, Kavindra Kumara; Izawa, Takeshi; Tennakoon, A.P.; Murakami, Hiroshi; Golbar, Hossain M.; Katou-Ichikawa, Chisa; Tanaka, Miyuu; Kuwamura, Mitsuru; Yamate, Jyoji

doi:10.1016/j.yexmp.2014.04.003

Cited by 68 publications

(90 citation statements)

References 67 publications

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“…However, we did not observe enhanced ex vivo NO production in our study. Third, under macrophage polarizing conditions, cirrhotic monocytes demonstrated enhanced M1 and M2 polarization relative to healthy donors, possibly due to the basal activation of these cells, similar to an observation of enhanced M1 and M2 macrophage polarization in a rat model of cirrhosis [52]. The clinical implications and etiopathogenesis of these observations merits further study.…”

Section: Discussionsupporting

confidence: 53%

Monocyte-derived dendritic cells from cirrhotic patients retain similar capacity for maturation/activation and antigen presentation as those from healthy subjects

Tanoue

Chang²,

Li³

et al. 2015

Cellular Immunology

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Few studies have investigated the impact of liver cirrhosis on dendritic cell function. The purpose of this study was to compare the activation and antigen-presentation capacity of monocyte-derived dendritic cells (MoDC) from cirrhotic patients (CIR) relative to healthy donors (HD). MoDC from CIR and HD were matured, phenotyped, irradiated and pulsed with 15mer peptides for two hepatocellular carcinoma-related antigens, alphafetoprotein and glypican-3, then co-cultured with autologous T-cells. Expanded T-cells were evaluated by interferon-gamma ELISPOT and intracellular staining. 15 CIR and 7 HD were studied. While CD14+ monocytes from CIR displayed enhanced M2 polarization, under MoDC-polarizing conditions, we identified no significant difference between HD and CIR in maturation-induced upregulation of co-stimulation markers. Furthermore, no significant differences were observed between CIR and HD in subsequent expansion of tumor antigen-specific IFNγ+ T-cells. Conclusion MoDCs isolated from cirrhotic individuals retain similar capacity for in vitro activation, maturation and antigen-presentation as those from healthy donors.

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Section: Discussionsupporting

confidence: 53%

Monocyte-derived dendritic cells from cirrhotic patients retain similar capacity for maturation/activation and antigen presentation as those from healthy subjects

Tanoue

Chang²,

Li³

et al. 2015

Cellular Immunology

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“…These studies also identified the weakly F4/80-immunopositive subsets as infiltrating monocyte-derived macrophages. In contrast, the number of IBA1, CD68 and galectin-3 positive macrophages increases upon liver injury 38, 39 . We observed depletion of F4/80-expressing macrophages in Bcs1l G/G livers but an increased number of IBA1-positive macrophages, the latter of which was reduced on KD.…”

Section: Discussionmentioning

confidence: 99%

Ketogenic diet attenuates hepatopathy in mouse model of respiratory chain complex III deficiency caused by a Bcs1l mutation

Purhonen

Rajendran

Mörgelin

et al. 2017

Sci Rep

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Mitochondrial disorders are among the most prevalent inborn errors of metabolism but largely lack treatments and have poor outcomes. High-fat, low-carbohydrate ketogenic diets (KDs) have shown beneficial effects in mouse models of mitochondrial myopathies, with induction of mitochondrial biogenesis as the suggested main mechanism. We fed KD to mice with respiratory chain complex III (CIII) deficiency and progressive hepatopathy due to mutated BCS1L, a CIII assembly factor. The mutant mice became persistently ketotic and tolerated the KD for up to 11 weeks. Liver disease progression was attenuated by KD as shown by delayed fibrosis, reduced cell death, inhibition of hepatic progenitor cell response and stellate cell activation, and normalization of liver enzyme activities. Despite no clear signs of increased mitochondrial biogenesis in the liver, CIII assembly and activity were improved and mitochondrial morphology in hepatocytes normalized. Induction of hepatic glutathione transferase genes and elevated total glutathione level were normalized by KD. Histological findings and transcriptome changes indicated modulation of liver macrophage populations by the mutation and the diet. These results reveal a striking beneficial hepatic response to KD in mice with mitochondrial hepatopathy and warrant further investigations of dietary modification in the management of these conditions in patients.

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“…Macrophage activation is an essential event that occurs in the liver in response to infection, injury or metabolic disease . Two different subsets of macrophages with distinct functions have been previously described in NAFLD . On the one hand, M1 macrophages have been shown to produce proinflammatory cytokines, including TNF‐α, IFN‐γ and IL‐1β in order to mediate liver injury.…”

Section: Discussionmentioning

confidence: 99%

“…Classically activated macrophages, M1 macrophages, produce proinflammatory cytokines, including interleukin (IL)‐1β and tumor necrosis factor alpha (TNF‐α). Alternatively, activated M2 macrophages promote the apoptosis of M1 macrophages through the secretion of IL‐10 and the activation of arginase, resulting in increased protection against NAFLD . M2 macrophages are subdivided into M2a, M2b and M2c depending on the type of stimulants.…”

Section: Introductionmentioning

confidence: 99%

IL‐25 protects against high‐fat diet‐induced hepatic steatosis in mice by inducing IL‐25 and M2a macrophage production

Zheng

Gong

et al. 2018

Immunol Cell Biol

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Interleukin (IL)‐25 is a cytokine that has previously been shown to have a protective role against nonalcoholic fatty liver disease (NAFLD), which is associated with the induction of M2 macrophage differentiation. However, the direct relationships between IL‐25 expression regulation, M2 induction and NAFLD remain unknown. In this study, we demonstrate that IL‐25 promotes hepatic macrophage differentiation into M2a macrophages both in vivo and in vitro via the IL‐13/STAT6 pathway. M2 macrophages that were differentiated in vitro were able to ameliorate high‐fat diet HFD‐induced hepatic steatosis. Furthermore, we found that IL‐25 treatment, both in vitro and in vivo, promotes direct binding of STAT6 to the IL‐25 gene promoter region. This binding of STAT6 in response to IL‐25 treatment also resulted in the increase of IL‐25 expression in hepatocytes. Together, these findings identify IL‐25 as a protective factor against HFD‐induced hepatic steatosis by inducing an increase of IL‐25 expression in hepatocytes and through promotion of M2a macrophage production.

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M1- and M2-macrophage polarization in rat liver cirrhosis induced by thioacetamide (TAA), focusing on Iba1 and galectin-3

Cited by 68 publications

References 67 publications

Monocyte-derived dendritic cells from cirrhotic patients retain similar capacity for maturation/activation and antigen presentation as those from healthy subjects

Monocyte-derived dendritic cells from cirrhotic patients retain similar capacity for maturation/activation and antigen presentation as those from healthy subjects

Ketogenic diet attenuates hepatopathy in mouse model of respiratory chain complex III deficiency caused by a Bcs1l mutation

IL‐25 protects against high‐fat diet‐induced hepatic steatosis in mice by inducing IL‐25 and M2a macrophage production

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