• Parasites, Hosts and Diseases
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• 제52권6호
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• pp.695-699
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• 2014

Chronic Opisthorchis viverrini-induced hepatobiliary disease is associated with significant leukocyte infiltration, including activated macrophages; however, the polarization of infiltrating macrophages remains to be fully characterized. In this study, we characterized macrophage polarization and phenotype in chronic O. viverrini-induced hepatobiliary disease in humans and hamsters using gene expression and histochemical analysis. Chronic O. viverrini infection and associated hepatobiliary diseases were associated with iron loaded M2-like macrophages in both humans and hamsters. This study provides suggestive evidence that iron loaded M2-like macrophages promote hepatobiliary disease in chronic O. viverrini infection.

• Advances in Traditional Medicine
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• 제7권3호
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• pp.229-234
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• 2007

In macrophages, nitric oxide (NO) is released as an inflammatory mediator and has been proposed to be an important modulator of many pathophysiological conditions including inflammation. In this study, we have examined the inhibition effects of NO production by 85% methanol extract of the flower of Pueraria thunbergiana (PF) in mouse macrophages. Extract of PF (1, 10, 100 ${\mu}g/ml$) inhibited NO production, inducible NO synthase and cyclooxygenase-2 expression in interferon-g and lipopolysaccharide-stimulated mouse peritoneal macrophages and it had no cytotoxicity. These data suggest that 85% methanol extract of PF might be useful in controlling macrophages mediated inflammatory disease.

• 동의생리병리학회지
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• 제21권2호
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• pp.479-484
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• 2007

The purpose of this research was to investigate effects of mixed extract of Ginseng Radix and Angelicae gigantis Radix on activity of murine splenocytes and macrophages. GAE (300 mg/kg) was administered p.o. for 7 days. GAE decreased the viability of murine splenocytes in vivo. Also, GAE enhanced the population of $Thy1^+$ cells in splenocytes and the population of splenic $CD4^+$ cells. Furthermore, GAE increased the production of ${\Upsilon}$-interferon from splenocytes. GAE enhanced the production of nitric oxide and the phagocytic activity of peritoneal macrophages. These results suggest that GAE regulates the immune response via activation of splenic Th1 cells and peritoneal macrophages.

• IMMUNE NETWORK
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• 제14권6호
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• pp.328-332
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• 2014

Dexamethasone (Dex) was shown to inhibit the differentiation, maturation, and antigen-presenting function of dendritic cells (DC) when added during DC generation or maturation stages. Here, we examined the direct effects of Dex on MHC-restricted antigen processing. Macrophages were incubated with microencapsulated ovalbumin (OVA) in the presence of different concentrations of Dex for 2 h, and the efficacy of OVA peptide presentation was evaluated using OVA-specific CD8 and CD4 T cells. Dex inhibited both class I- and class II-restricted presentation of OVA to T cells; this inhibitory effect on antigen presentation was much more potent in immature macrophages than in mature macrophages. The presentation of the exogenously added OVA peptide SIINFEKL was not blocked by Dex. In addition, short-term treatment of macrophages with Dex had no discernible effects on the phagocytic activity, total expression levels of MHC molecules or co-stimulatory molecules. These results demonstrate that Dex inhibits intracellular processing events of phagocytosed antigens in macrophages.

• Biomolecules & Therapeutics
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• 제10권4호
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• pp.224-229
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• 2002

Triazine herbicide has been reported to directly suppress the immune response. In the present study, we examined various functions of murine peritoneal macrophages that were isolated and stimulated with LPS after simazine (300 and 600 mg/kg body weight), a triazine herbicide, was administered every day for 4 weeks. Simazine decreased the capacity of phagocytosis, compared to those of carboxymethylcellulose (CMC)-treated control group. In addition, the production of NO and TNF-$\alpha$ was decrcased in macrophages of simazinetreated mice. However, the production of hydrogen peroxide ($H_{2}O_{2}$) was not altered. In vitro tumoricidal activity of in vivo simazine-treated macrophages was reduced against target cell. B 16 melanoma. Taken together, these results suggested that simazine might have the immunosuppressive effect on macrophages after in vivo exposure, which was related to the reduction of tumoricidal activity.

• 한국식품영양과학회지
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• 제26권6호
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• pp.1252-1257
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• 1997

In order to investigate the immunomodulatory mechanism of white ginseng, the effects of total saponin of Ginsenoside Rb$_2$component on the phagocytosis and reactive oxygen intermediate(ROI) production of mouse peritoneal macrophages were studied. Both phagocytosis assay nitrobluetetrazolium reduction test showed 20$\mu\textrm{g}$/ml concentration of total saponin significantly increased the activity of phagocytosis and production of ROI. Also cytokine gene expression of the macrophages was analyzed using reverse transcription polymerase chain reaction. In the RT-PCR assay, 20$\mu\textrm{g}$/ml concentration of either total saponin or Ginsenoside Rb$_2$increased IL-1 and TNF expression of the macrophages.

• BMB Reports
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• 제52권6호
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• pp.360-372
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• 2019

Macrophages play an essential role not only in mediating the first line of defense but also in maintaining tissue homeostasis. In response to extrinsic factors derived from a given tissue, macrophages activate different functional programs to produce polarized macrophage populations responsible for inducing inflammation against microbes, removing cellular debris, and tissue repair. However, accumulating evidence has revealed that macrophage polarization is pivotal in the pathophysiology of metabolic syndromes and cancer, as well as in infectious and autoimmune diseases. Recent advances in transcriptomic and metabolomic studies have highlighted the link between metabolic rewiring of macrophages and their functional plasticity. These findings imply that metabolic adaption to their surrounding microenvironment instructs activation of macrophages with functionally distinct phenotypes, which in turn probably leads to the pathogenesis of a wide spectrum of diseases. In this review, we have introduced emerging concepts in immunometabolism with focus on the impact on functional activation of macrophages. Furthermore, we have discussed the implication of macrophage plasticity on the pathogenesis of metabolic syndromes and cancer, and how the disease microenvironment manipulates macrophage metabolism with regard to the pathophysiology.

• BMB Reports
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• 제55권11호
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• pp.519-527
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• 2022

Macrophage activation has long been implicated in a myriad of human pathophysiology, particularly in the context of the dysregulated capacities of an unleashing intracellular or/and extracellular inflammatory response. A growing number of studies have functionally coupled the macrophages' inflammatory capacities with dynamic metabolic reprogramming which occurs during activation, albeit the results have been mostly interpreted through classic metabolism point of view; macrophages take advantage of the rewired metabolism as a source of energy and for biosynthetic precursors. However, a specific subset of metabolic products, namely immune-modulatory metabolites, has recently emerged as significant regulatory signals which control inflammatory responses in macrophages and the relevant extracellular milieu. In this review, we introduce recently highlighted immuno-modulatory metabolites, with the aim of understanding their physiological and pathological relevance in the macrophage inflammatory response.

• Anatomy and Cell Biology
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• 제55권1호
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• pp.14-19
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• 2022

At present, chronic liver disease accounts for approximately 2 million deaths per year worldwide. Liver injury induces a series of events causing inflammation. Chronic inflammation ends in liver fibrosis. A stage of fibrinolysis occurs on stopping insult. Kupffer cells play their role to initiate inflammatory responses, while infiltrating monocyte-derived macrophages have a role both in chronic inflammation and fibrosis and in fibrosis resolution. Ly-6C high expressing monocytes act during fibrogenesis, while Ly-6C low expressing monocytes are restorative macrophages which promote resolution of fibrosis after end of the injury. Recent studies have identified new phenotypes, such as metabolically activated M, oxidized, which may have a role in fatty liver diseases.

• Natural Product Sciences
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• 제14권3호
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• pp.206-213
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• 2008

This study was designed to investigate the anti-inflammatory effects of mangiferin isolated from the rhizome of Anemarrhena asphodeloides, a natural polyphenol, on lipopolysaccharide (LPS)-treated RAW 264.7 macrophages. Mangiferin dose-dependently inhibited LPS-induced nitric oxide (NO) and prostaglandin $E_2\;(PGE_2)$ productions in RAW 264.7 macrophages and peritoneal macrophages isolated from C57BL/6 mice. Consistent with these data, mangiferin suppressed the LPS-induced expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein and mRNA levels in a concentration-dependent manner, as determined by Western blotting and RT-PCR, respectively. In addition, the release of tumor necrosis $factor-{\alpha}$($TNF-{\alpha}$) and interleukin-6 (IL-6), and the mRNA expression levels of these cytokines were reduced by mangiferin in a dose-dependent manner. Moreover, mangiferin effectively inhibited the transcriptional activation of nuclear factor-kappa B $(NF-{\kappa}B)$. These results suggest that the anti-inflammatory properties of mangiferin are caused by iNOS, COX-2, $TNF-{\alpha}$, and IL-6 down-regulation due to $(NF-{\kappa}B)$ inhibition in RAW 264.7 macrophages.