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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2018.1
- 수록면
- 65 - 73 (9page)
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초록· 키워드
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Pretreatment of low-dose lipopolysaccharide (LPS) induces a hyporesponsive state to subsequent secondary challenge with high-dose LPS in innate immune cells, whereas super-low-dose LPS results in augmented expression of pro-inflammatory cytokines. However, little is known about the difference between super-low-dose and lowdose LPS pretreatments on immune cell-mediated inflammatory and hepatic acute-phase responses to secondary LPS. In the present study, RAW 264.7 cells, EL4 cells, and Hepa-1c1c7 cells were pretreated with super-low-dose LPS (SL-LPS: 50 pg/mL) or low-dose LPS (L-LPS: 50 ng/mL) in fresh complete medium once a day for 2~3 days and then cultured in fresh complete medium for 24 hr or 48 hr in the presence or absence of LPS (1~10 μg/mL) or concanavalin A (Con A). SL-LPS pretreatment strongly enhanced the LPS-induced production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, TNF-α/IL-10, prostaglandin E2 (PGE2), and nitric oxide (NO) by RAW 264.7 cells compared to the control, whereas L-LPS increased IL-6 and NO production only. SL-LPS strongly augmented the Con A-induced ratios of interferon (IFN)-γ/IL-10 in EL4 cells but decreased the LPS-induced ratios of IFN-γ/IL-10 compared to the control, while L-LPS decreased the Con A- and LPS-induced ratios of IFN-γ/IL-10. SL-LPS enhanced the LPS-induced production of IL-6 by Hepa1c1c-7 cells compared to the control, while L-LPS increased IL-6 but decreased IL-1β and C reactive protein (CRP) levels. SL-LPS pretreatment strongly enhanced the LPS-induced production of TNF-α, IL-6, IL-10, PGE2, and NO in RAW 264.7 cells, and the IL-6, IL-1β, and CRP levels in Hepa1c1c-7 cells, as well as the ratios of IFN-γ/IL-10 in LPS- and Con A-stimulated EL4 cells compared to L-LPS. These findings suggest that pre-conditioning of SL-LPS may contribute to the mortality to secondary infection in sepsis rather than pre-conditioning of L-LPS.
목차
Abstract
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
참고문헌 (39)
참고문헌 신청
Alexander, C. / 2001 / Bacterial lipopolysaccharides and innate immunity / J. Endotoxin Res. 7:167~202
Patel, P.N. / 2015 / Human experimental endotoxemia in modeling the pathophysiology, genomics, and therapeutics of innate immunity in complex cardiometabolic diseases / Arterioscler. Thromb. Vasc. Biol. 35:525~534
Offenbacher, S. / 1999 / Induction of prostaglandin release from macrophages by bacterial endotoxin / Clin. Infect. Dis. 28:505~513
Kawai, T. / 2007 / Signaling to NF-kappaB by Toll-like receptors / Trends Mol. Med. 13:460~469
Biswas, S.K. / 2009 / Endotoxin tolerance: new mechanisms, molecules and clinical significance / Trends Immunol. 30:475~487
Patel, P.N. / 2015 / Human experimental endotoxemia in modeling the pathophysiology, genomics, and therapeutics of innate immunity in complex cardiometabolic diseases / Arterioscler. Thromb. Vasc. Biol. 35:525~534
Offenbacher, S. / 1999 / Induction of prostaglandin release from macrophages by bacterial endotoxin / Clin. Infect. Dis. 28:505~513
Kawai, T. / 2007 / Signaling to NF-kappaB by Toll-like receptors / Trends Mol. Med. 13:460~469
Biswas, S.K. / 2009 / Endotoxin tolerance: new mechanisms, molecules and clinical significance / Trends Immunol. 30:475~487
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UCI(KEPA) : I410-ECN-0101-2018-513-001743758