scholarly journals Dibenzoylmethane, a Component of Licorice, Suppresses Monocyte-to-Macrophage Differentiation and Inflammatory Responses in Human Monocytes and Mouse Macrophages

2018 ◽  
Vol 41 (8) ◽  
pp. 1228-1236 ◽  
Author(s):  
Bobin Kang ◽  
Joo Hyoun Kim ◽  
Chae Young Kim ◽  
Jungil Hong ◽  
Hyeon-Son Choi
Keyword(s):  
Inflammatory Responses ◽  
Human Monocytes ◽  
Macrophage Differentiation ◽  
Mouse Macrophages

scholarly journals Biochemical and genetic studies of the apoprotein E secreted by mouse macrophages and human monocytes.

1982 ◽  
Vol 257 (16) ◽  
pp. 9788-9795 ◽  
Author(s):  
S K Basu ◽  
Y K Ho ◽  
M S Brown ◽  
D W Bilheimer ◽  
R G Anderson ◽  
...  
Keyword(s):  
Human Monocytes ◽  
Genetic Studies ◽  
Mouse Macrophages ◽  
Apoprotein E

scholarly journals Inhibition of Inflammatory Responses by Centella asiatica via Suppression of IRAK1-TAK1 in Mouse Macrophages

2020 ◽  
Vol 48 (05) ◽  
pp. 1103-1120
Author(s):  
Young-Chang Cho ◽  
Huong Lan Vuong ◽  
Jain Ha ◽  
Sewoong Lee ◽  
Jiyoung Park ◽  
...  
Keyword(s):  
Transforming Growth Factor ◽  
Inflammatory Responses ◽  
Centella Asiatica ◽  
Prostaglandin E ◽  
Methanol Fraction ◽  
Raw 264.7 Macrophages ◽  
Inflammatory Mechanism ◽  
Mouse Macrophages ◽  
Mitogen Activated Protein ◽  
Anti Inflammatory

Centella asiatica (L.) Urb. (C. asiatica) has been widely treated for inflammation-related diseases in China for thousands of years. While C. asiatica showed relevant effects as traditional medicine, the mechanism of C. asiatica suppressing inflammation has not been thoroughly investigated. Therefore, this study was conducted to reveal the anti-inflammatory mechanism of methanol fraction from C. asiatica (MCA) at the molecular level in murine macrophages. Levels of inflammation-related mediators were observed with treatment of MCA. MCA significantly suppressed nitric oxide production and iNOS expression in RAW 264.7 macrophages. Prostaglandin E2 production was alleviated by MCA via the downregulation of cyclooxygenase-2. MCA treatment also reduced pro-inflammatory tumor necrosis factor-[Formula: see text] and interleukin (IL)-6 levels. LPS/D-GalN-induced acute hepatitis in mouse was alleviated by MCA treatment. In addition, MCA decreased the phosphorylation of inhibitory [Formula: see text]B[Formula: see text] (I[Formula: see text]B[Formula: see text]) at Ser32/36 and thereby blocked I[Formula: see text]B[Formula: see text] degradation. TXY motif phosphorylation in the activation loops of mitogen-activated protein kinases (MAPKs) was also suppressed by MCA treatment. Further investigation revealed that MCA inhibited transforming growth factor-[Formula: see text]-activated kinase 1 (TAK1) phosphorylation and IL-1 receptor-associated kinase (IRAK1) degradation, the upstream kinases activating nuclear factor [Formula: see text]B and MAPKs. Taken together, MCA exhibited anti-inflammatory properties via the downregulation of IRAK1-TAK1 signaling pathways.

scholarly journals Modulatory effect of antibiotics on cytokine production by human monocytes in vitro.

1996 ◽  
Vol 40 (6) ◽  
pp. 1366-1370 ◽  
Author(s):  
K Morikawa ◽  
H Watabe ◽  
M Araake ◽  
S Morikawa
Keyword(s):  
Antimicrobial Agents ◽  
Inflammatory Responses ◽  
Interleukin 1 ◽  
Immunomodulatory Activity ◽  
Lymphocyte Function ◽  
Dependent Manner ◽  
Human Monocytes ◽  
Concentration Dependent Manner ◽  
Cytokine Synthesis

Some antimicrobial agents have been reported to modify the host immune and inflammatory responses both in vivo and in vitro. Fosfomycin (FOM) and clarithromycin (CAM) have immunomodulatory activity on human lymphocyte function. In the present study, we examined the effects of FOM and CAM on cytokine synthesis by lipopolysaccharide (LPS)-stimulated human monocytes in comparison with that of dexamethasone in vitro. The three drugs demonstrated positive or negative effects on the synthesis of various cytokines by LPS-primed monocytes. They suppressed the synthesis of tumor necrosis factor alpha, interleukin 1 alpha (IL-1 alpha), IL-1 beta, the IL-1 receptor antagonist, and granulocyte-macrophage colony-stimulating factor in a concentration-dependent manner at concentrations between 1.6 and 40 micrograms/ml. On the contrary, the drugs showed different actions on the synthesis of IL-6 and IL-10. Namely, FOM enhanced both IL-6 and IL-10 synthesis, CAM enhanced only IL-10 synthesis, but dexamethasone deeply suppressed the synthesis of both cytokines. These data indicate that antibacterial agents may modify acute-phase inflammatory responses through their effects on cytokine synthesis by monocytes.

scholarly journals Inhibition of nicotinamide phosphoribosyltransferase modifies LPS-induced inflammatory responses of human monocytes

2011 ◽  
Vol 18 (3) ◽  
pp. 518-530 ◽  
Author(s):  
Erik Schilling ◽  
Janine Wehrhahn ◽  
Carina Klein ◽  
Nora Raulien ◽  
Uta Ceglarek ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Human Monocytes ◽  
Nicotinamide Phosphoribosyltransferase

Short-term Cytotoxic and Inflammatory Responses of Human Monocytes to Stainless Steel Fibre Networks

2012 ◽  
Vol 1417 ◽  
Author(s):  
Rose L. Spear ◽  
Roger A. Brooks ◽  
Athina E. Markaki
Keyword(s):  
Stainless Steel ◽  
Steel Fibre ◽  
Volume Fraction ◽  
Inflammatory Responses ◽  
Fibre Volume Fraction ◽  
Human Monocyte ◽  
Positive Control ◽  
Fibre Volume ◽  
Human Monocytes ◽  
Tnf Α

ABSTRACTThe aim of the current work was to examine the human monocyte response to 444 ferritic stainless steel fibre networks. 316L austenitic fibre networks, of the same fibre volume fraction, were used as control surfaces. Fluorescence and scanning electron microscopies suggest that the cells exhibited a good degree of attachment and penetration throughout both networks. Lactate Dehydrogenase (LDH) and TNF-α releases were used as indicators of cytotoxicity and inflammatory responses respectively. LDH release indicated similar levels of monocyte viability when in contact with the 444 and 316L fibre networks. Both networks elicited a low level secretion of TNF-α, which was significantly lower than that of the positive control wells containing zymosan. Collectively, the results suggest that 444 ferritic and 316L austenitic networks induced similar cytotoxic and inflammatory responses from human monocytes.

scholarly journals Regulation of Notch 1 signaling in THP-1 cells enhances M2 macrophage differentiation

2014 ◽  
Vol 307 (11) ◽  
pp. H1634-H1642 ◽  
Author(s):  
Reetu D. Singla ◽  
Jing Wang ◽  
Dinender K. Singla
Keyword(s):  
Notch Signaling ◽  
Proinflammatory Cytokine ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Macrophage Polarization ◽  
Cellular Stress ◽  
Culture Conditions ◽  
M2 Macrophage ◽  
Macrophage Differentiation ◽  
Anti Inflammatory

Macrophage polarization is emerging as an important area of research for the development of novel therapeutics to treat inflammatory diseases. Within the current study, the role of Notch1R in macrophage differentiation was investigated as well as downstream effects in THP-1 monocytes cultured in “inflammation mimicry” media. Interference of Notch signaling was achieved using either the pharmaceutical inhibitor DAPT or Notch1R small interfering RNA (siRNA), and Notch1R expression, macrophage phenotypes, and anti- and proinflammatory cytokine expression were evaluated. Data presented show that Notch1R expression on M1 macrophages as well as M1 macrophage differentiation is significantly elevated during cellular stress ( P < 0.05). However, under identical culture conditions, interference to Notch signaling via Notch1R inhibition mitigated these results as well as promoted M2 macrophage differentiation. Moreover, when subjected to cellular stress, macrophage secretion of proinflammatory cytokines was significantly heightened ( P < 0.05). Importantly, Notch1R inhibition not only diminished proinflammatory cytokine secretion but also enhanced anti-inflammatory protein release ( P < 0.05). Our data suggest that Notch1R plays a pivotal role in M1 macrophage differentiation and heightened inflammatory responses. Therefore, we conclude that inhibition of Notch1R and subsequent downstream signaling enhances monocyte to M2 polarized macrophage outcomes and promotes anti-inflammatory mediation during cellular stress.

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