Phosphatidylserine-containing liposomes suppress inflammatory bone loss by ameliorating the cytokine imbalance provoked by infiltrated macrophages.
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...Furthermore, recent studies have shown that liposome administration can alter macrophage phenotype in vivo in part by induction of ERK signaling after ingestion (53, 54)....
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...[77] suggests that this effect is due to increased IL-10 production by macrophages....
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...In vivo, PSLs have been described to promote the resolution of inflammation by modulating macrophage function in a model for inflammatory bone loss and myocardial infarction [31,33]....
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...In vitro, clearance of apoptotic cells and PSLs skews macrophages towards a tolerogenic phenotype [21,23,29-35]....
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55 citations
References
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"Phosphatidylserine-containing lipos..." refers result in this paper
...This was consistent with the fact that IL-1 β is essential for promoting Th17 cell differentiation and IL-17 production by the differentiated Th17 cells...
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1,705 citations
"Phosphatidylserine-containing lipos..." refers background in this paper
...E-mails: zhouw@dent.kyushu-u.ac.jp or nakan@dent.kyushu-u.ac.jp Laboratory Investigation (2011) 91, 921–931 & 2011 USCAP, Inc All rights reserved 0023-6837/11 $32.00 www.laboratoryinvestigation.org | Laboratory Investigation | Volume 91 June 2011 921 (RANKL) and RANK, which have essential roles in differentiation and the activity of osteoclasts.18 Among pro-inflammatory cytokines, interleukin (IL)-1b is a master regulator of inflammation and inflammatory bone loss, because it can induce other pro-inflammatory cytokines.19,20 Recently, much attention has been paid to IL-17 as a crucial cytokine for inflammatory osteoclastic bone loss because of its marked induction of RANKL.21 Indeed, high levels of IL-1b and IL-17 are found in the plasma and synovial tissues of rheumatoid arthritis (RA) patients, and combined blockade of IL-1b and IL-17 receptors significantly inhibited the rheumatoid arthritic osteoporosis.22 Among anti-inflammatory mediators, including TGF-b1 and PGE2, IL-10 is known as the strongest feedback mediator of inflammatory bone loss.23,24 The paw volume increase of adjuvant arthritic (AA) rat, an animal model of RA,25–27 occurs in two stages: namely an acute inflammation stage from 10 to 21 days after complete Freund’s adjuvant (CFA) injection, and the chronic bone/ joint destruction stage thereafter....
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...First, PSLs decreased the expression levels of IL-1b and IL-17, which can promote the expression of RANKL.38,39 Second, PSL-induced IL-10, which strongly inhibited the expression of RANKL/RANK.23,37 Third, PSLs are phagocytosed by the osteoclast precursor to directly decrease the expression of RANK by osteoclast precursor and the production of RANKL in cultured rat bone marrow cells.17 Therefore, it is considered that the inhibitory effect of PSLs on the trabecular bone loss in AA rats completely depends on the inhibition of the RANKL/RANK pathway....
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...a crucial cytokine for inflammatory osteoclastic bone loss because of its marked induction of RANKL.(21) Indeed, high levels of IL-1b and IL-17 are found in the plasma and...
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"Phosphatidylserine-containing lipos..." refers background in this paper
...PS-dependent phagocytosis of apoptotic cells is believed to trigger the secretion of anti-inflammatory cytokines and restrains that of pro-inflammatory cytokines from macrophages(8,9) and dendritic cells.(10,11) Recently, we and others have found that PS-containing liposomes (PSLs) mimic apoptotic cells to...
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