Munkyong Pae

Prof. Munkyong Pae

orcid

Research Focus & Metrics

Academic Career Length

21Years (2006-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 April 2016 in Cell Metabolism
Verified
Journal Article
Closed access
BLByung-Cheol Lee
Byung-Cheol Lee
MKMyung-Sunny Kim
Myung-Sunny Kim
MPMunkyong Pae
Munkyong Pae
YYYasuhiko Yamamoto
Yasuhiko Yamamoto
DEDelphine Eberlé
Delphine Eberlé
JLJongsoon Lee
Jongsoon Lee

1 October 2007 in The Journal of Immunology
Verified
Journal Article
Open access
PDF file
DWDayong Wu
Dayong Wu
ZRZhihong Ren
Zhihong Ren
MPMunkyong Pae
Munkyong Pae
Weimin GuoWeimin Guo
Weimin Guo
XCXuelin Cui
Xuelin Cui
SMSimin Nikbin Meydani
Simin Nikbin Meydani
Obesity is a leading risk factor for type 2 diabetes (T2D). Aging is associated with an increase in T2D incidence, which is not totally explained by the much lower prevalence of obesity in the elderly. Low-grade inflammation in adipose tissue (AT) contributes to insulin resistance and T2D. Thus, we determined whether inflammatory responses are up-regulated with age in AT. The results showed that visceral AT from old C57BL mice had significantly higher mRNA expression of the proinflammatory cytokines IL-1β, IL-6, TNF-α, and COX-2 and lower expression of anti-inflammatory PPAR-γ than those of young mice. We further showed that adipocytes (AD) and not stromal vascular cells including macrophages (Mφ) were the cells responsible for this higher inflammatory state of the aged AT, suggesting that the age-associated increase in AT inflammation is distinguished from that seen in obesity, in which Mφ are the main contributors. However, peritoneal Mφ of either age (young or old) produced more TNF-α and IL-6 after incubation in old AD-conditioned medium compared with young AD-conditioned medium. This suggests that in addition to producing more inflammatory cytokines, AD from old mice induce a higher inflammatory response in other cells. Sphingolipid ceramide was higher in old compared with young AD. Reducing ceramide levels or inhibiting NF-κB activation decreased cytokine production, whereas the addition of ceramide increased cytokine production in young AD to a level comparable to that seen in old AD, suggesting that ceramide-induced activation of NF-κB plays a key role in AT inflammation.

1 February 2012 in Molecular Aspects of Medicine
Verified
Journal Article
Closed access
DWDayong Wu
Dayong Wu
JWJunpeng Wang
Junpeng Wang
MPMunkyong Pae
Munkyong Pae
SMSimin Nikbin Meydani
Simin Nikbin Meydani

20 June 2013 in Food & Function
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Journal Article
Closed access
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MPMunkyong Pae
Munkyong Pae
DWDayong Wu
Dayong Wu
Consuming green tea or its active ingredient, epigallocatechin-3-gallate (EGCG), has been shown consistently to benefit the healthy functioning of several body systems. In the immune system specifically, accumulating evidence has revealed an immunomodulating effect of green tea/EGCG. Several types of immune cells in both the innate and adaptive immune systems are known to be affected in varying degrees by green tea/EGCG. Among them, the dramatic effect on T cell functions has been repeatedly demonstrated, including T cell activation, proliferation, differentiation, and production of cytokines. In particular, dysregulated T cell function with respect to different subsets of CD4+ T cells is a critical pathogenic factor in the development of autoimmune inflammatory diseases. Recent studies have shown that EGCG affects the differentiation of naïve CD4+ T cells into different effector subsets in a way that would be expected to favorably impact autoimmunity. Consistent with these findings, studies using animal models of autoimmune diseases have reported disease improvement in animals treated with green tea/EGCG. Altogether, these studies identify and support the use of EGCG as a potential therapeutic agent in preventing and ameliorating T cell-mediated autoimmune diseases. Given the paucity of information in human studies, the translational value of these findings needs to be verified in future research.

1 February 2012
Verified
Journal Article
Closed access
MPMunkyong Pae
Munkyong Pae
SMSimin Nikbin Meydani
Simin Nikbin Meydani
DWDayong Wu
Dayong Wu

1 June 2007 in The Journal of Nutrition
Verified
Journal Article
Open access
PDF file
DWDayong Wu
Dayong Wu
MPMunkyong Pae
Munkyong Pae
ZRZhihong Ren
Zhihong Ren
ZGZhuyan Guo
Zhuyan Guo
DSDonald Smith
Donald Smith
SMSimin Nikbin Meydani
Simin Nikbin Meydani
Mushrooms are reported to possess antitumor, antiviral, and antibacterial properties. These effects of mushrooms are suggested to be due to their ability to modulate immune cell functions. However, a majority of these studies evaluated the effect of administering extracts of exotic mushrooms through parental routes, whereas little is known about the immunological effect of a dietary intake of white button mushrooms, which represent 90% of mushrooms consumed in the U.S. In this study, we fed C57BL/6 mice a diet containing 0, 2, or 10% (wt/wt) white button mushroom powder for 10 wk and examined indices of innate and cell-mediated immunity. Mushroom supplementation enhanced natural killer (NK) cell activity, and IFNγ and tumor necrosis factor-α (TNFα) production, but only tended to increase IL-2 (P = 0.09) and did not affect IL-10 production by splenocytes. There were significant correlations between NK activity and production of IFNγ (r = 0.615, P < 0.001) and TNFα (r = 0.423, P = 0.032) in splenocytes. Mushroom supplementation did not affect macrophage production of IL-6, TNFα, prostaglandin E2, nitric oxide, and H2O2, nor did it alter the percentage of total T cells, helper T cells (CD4+), cytotoxic or suppressive T cells (CD8+), regulatory T cells (CD4+/CD25+), total B cells, macrophages, and NK cells in spleens. These results suggest that increased intake of white button mushrooms may promote innate immunity against tumors and viruses through the enhancement of a key component, NK activity. This effect might be mediated through increased IFNγ and TNFα production.