• The Korean Journal of Physiology and Pharmacology
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• 제22권1호
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• pp.1-15
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• 2018

Inflammasomes are intracellular multiprotein complexes that coordinate anti-pathogenic host defense during inflammatory responses in myeloid cells, especially macrophages. Inflammasome activation leads to activation of caspase-1, resulting in the induction of pyroptosis and the secretion of pro-inflammatory cytokines including interleukin $(IL)-1{\beta}$ and IL-18. Although the inflammatory response is an innate host defense mechanism, chronic inflammation is the main cause of rheumatic diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), and $Sj{\ddot{o}}gren^{\prime}s$ syndrome (SS). Since rheumatic diseases are inflammatory/autoimmune disorders, it is reasonable to hypothesize that inflammasomes activated during the inflammatory response play a pivotal role in development and progression of these diseases. Indeed, previous studies have provided important observations that inflammasomes are actively involved in the pathogenesis of inflammatory/autoimmune rheumatic diseases. In this review, we summarize the current knowledge on several types of inflammasomes during macrophage-mediated inflammatory responses and discuss recent research regarding the role of inflammasomes in the pathogenesis of inflammatory/autoimmune rheumatic diseases. This avenue of research could provide new insights for the development of promising therapeutics to treat inflammatory/autoimmune rheumatic diseases.

• Food Science and Biotechnology
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• 제18권3호
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• pp.813-817
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• 2009

The effect of 4 seaweed extracts (Desmarestia viridis, Dictyopteris divaricata, Scytosiphon lomentaria, and Ishige okamurae) on pro-inflammatory mediators as well as nuclear factor $(NF)-{\kappa}B$ in the stimulated Raw 264.7 cells was investigated. They reduced iNOS and interlukin $(IL)-1{\beta}$ expressions at transcription level. Of those, 3 extracts (D. divaricata, I. okamurae, and S. lomentaria) inhibited the COX-2 expression at translation level. $I{\kappa}B-{\alpha}$ degradation was inhibited by D. divaricata and S. lomentaria extracts. Therefore, we concluded that the extracts from D. divaricata and S. lomentaria could inhibit the activation of murine macrophage through the blocking of $NF-{\kappa}B$ activation.

• Biomolecules & Therapeutics
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• 제8권3호
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• pp.235-240
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• 2000

Antitumor effect of LC43, a protein-bound ploysaccharide (M.W. 43 kDa) that was purified from intergeneric protoplast fusant of Lentinus edodes and Coriolus versicolor, was elucidated against mouse sarcoma 180 cell in vitro and in vivo. By injecting LC43 into ICR mice bearing solid or ascitic sarcoma 180, tumor regression and survival rates were investigated. To examine the effects of LC43 on immunopotentiation activity. immunoorgan weight, B cell differentiation, T cell activity and macrophage activation were determined. LC43 showed antitumor effects against both solid tumor and ascitic tumor of sarcoma 180. It did not change significantly the immunoorgan weight but potentiated immune responses such as B cell differentiation and the release of superoxide anion from macrophages. These results suggest that the protein-bound polysaccharide of LC43 exhibited antitumor activities through the activation of immune-related cells and acted as an immunmodulator.

• Archives of Pharmacal Research
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• 제15권2호
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• pp.146-151
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• 1992

The aim of this study was to evaluate capability of pertussis toxin (PT) to active mouse macrophages. The investigations were undertaken to determine whether the role played by this toxin required the A-protomer of the toxin to ADP-ribosylate a guanine nucleotide binding protein (a class I activity) or was dependent on the binding of B-oligomer of the toxin to the surface of target cells (a Class II activity). The results of these experiments have established that the mechanism of macrophage activation with PT seems to be dependent upon a Class II activity of the toxin.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.258.2-258.2
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• 2002

In our previous study. we reported that PG. a polysaccharide isolated from Plyatycodon grandiflorum, activated macrophages and B cells. but not T cells. Here. we investigated in more detail the mechanism of action of PG in macrophage activation. Since PG cannot penetrate cells due to the large molecular mass, it should bind to membrane receptors of macrophages. We showed that some antibodies to cell surface molecules (CD14, CD11b. TLR2, and TLR4) inhibited RAW264.7 macrophage activation, suggesting the possible binding sites of PG. (omitted)

• 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.

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2023년도 임시총회 및 춘계학술대회
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• pp.42-42
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• 2023

Paeonia lactiflora roots (PLR) are a traditional medicinal plant used to treat inflammatory diseases. Recently, PLR has been reported to increase the secretion of immune regulatory factors and enhance phagocytic activity in macrophages. Therefore, in this study, we compared the macrophage activation induced by PLR under different extraction conditions. PLR extracts at temperatures ranging from 4℃ to 60℃ increased the secretion of immune regulatory factors, but the secretion slightly decreased at 80℃. Under time-based extraction conditions at 60℃, immune regulatory factor secretion by PLR extracts was similar from 1 to 24 hours. Therefore, considering the overall results of this study, extracting PLR at 60℃ for 1 hour is considered the optimal condition for macrophage activation.

• 대한약학회:학술대회논문집
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• 대한약학회 2001년도 Proceedings of the Pharmaceutical Society of Korea
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• pp.148.2-149
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• 2001

• Journal of Microbiology and Biotechnology
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• 제32권11호
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• pp.1406-1415
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• 2022

The formation of macrophage foam cells stimulated by oxidized low-density lipoprotein (ox-LDL) is deemed an important cause of atherosclerosis. Transcription factor Yin Yang 1 (YY1), which is a universally expressed multifunctional protein, is closely related to cell metabolism disorders such as lipid metabolism, sugar metabolism, and bile acid metabolism. However, whether YY1 is involved in macrophage inflammation and lipid accumulation still remains unknown. After mouse macrophage cell line RAW264.7 cells were induced by ox-LDL, YY1 and proprotein convertase subtilisin/kexin type 9 (PCSK9) expressions were found to be increased while low-density lipoprotein receptor (LDLR) expression was lowly expressed. Subsequently, through reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blot analysis, Oil Red O staining and cholesterol quantification, it turned out that silencing of YY1 attenuated the inflammatory response and lipid accumulation in RAW264.7 cells caused by ox-LDL. Moreover, results from the JASPAR database, chromatin immunoprecipitation (ChIP) assay, luciferase reporter assay and Western blot analysis suggested that YY1 activated PCSK9 by binding to PCSK9 promoter and modulated the expression of LDLR in the downstream of PCSK9. In addition, the results of functional experiments demonstrated that the inhibitory effects of YY1 interference on ox-LDL-mediated macrophage inflammation and lipid accumulation were reversed by PCSK9 overexpression. To sum up, YY1 depletion inhibited its activation of PCSK9, thereby reducing cellular inflammatory response, cholesterol homeostasis imbalance, and lipid accumulation caused by ox-LDL.