Phosphatidylserine-containing liposomes suppress inflammatory bone loss by ameliorating the cytokine imbalance provoked by infiltrated macrophages.
TLDR
PSL-induced different influence on the activities of p38 MAPK and ERK is a likely underlying mechanism for phenotypic change of infiltrated macrophages after the phagocytosis of PSLs, resulting in the inhibition of inflammatory bone loss.About:
This article is published in Laboratory Investigation.The article was published on 2011-06-01 and is currently open access. It has received 52 citations till now. The article focuses on the topics: Interleukin 10 & Phagocytosis.read more
Citations
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Wu-Tou Decoction in Rheumatoid Arthritis: Integrating Network Pharmacology and In Vivo Pharmacological Evaluation.
Qingqing Guo,Kang Zheng,Danping Fan,Yukun Zhao,Yukun Zhao,Li Li,Yanqin Bian,Xuemei Qiu,Xue Liu,Ge Zhang,Chaoying Ma,Xiaojuan He,Xiaojuan He,Aiping Lu,Aiping Lu +14 more
TL;DR: It was demonstrated in this research that WTD played a role in inhibiting inflammatory response in RA which was closely connected with the modulation effect of WTD on CCR5 signaling pathway in macrophages.
Journal ArticleDOI
“Eat me” imaging and therapy
TL;DR: Use of phosphatidylserine (PtdSer), the well-known "eat-me" signal, in nanoparticle-based therapeutics making them highly desirable "meals" for phagocytic immune cells is examined.
Journal ArticleDOI
Therapeutic applications of reconstituted HDL: When structure meets function
TL;DR: Current knowledge of structure-function relationships in rHDL formulations is summarized, with a focus on phosphatidylserine and other negatively-charged phospholipids, and their potential for the development of HDL-based therapies highlighted.
Journal ArticleDOI
Islet Macrophages Shift to a Reparative State following Pancreatic Beta-Cell Death and Are a Major Source of Islet Insulin-like Growth Factor-1
Dominika Nackiewicz,Meixia Dan,Madeleine Speck,Samuel Z. Chow,Yi-Chun Chen,J. Andrew Pospisilik,C. Bruce Verchere,Jan A. Ehses,Jan A. Ehses +8 more
TL;DR: It is found that following streptozotocin (STZ)-induced beta-cell death, mouse islet macrophages had increased Igf1 expression, decreased proinflammatory cytokine expression, and transcriptome changes consistent with macrophage undergoing efferocytosis and having an enhanced state of metabolism.
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Alteration of IL-17 Related Protein Expressions in Experimental Autoimmune Myocarditis and Inhibition of IL-17 by IL-10-Ig Fusion Gene Transfer
Haruo Hanawa,He Chang,Tsuyoshi Yoshida,Manabu Hayashi,Kiminori Kato,Makoto Kodama,Yoshifusa Aizawa +6 more
TL;DR: IL-17 produced by Th17 plays an important role in the pathogenesis of rat EAM, and IL-17 inhibition might be a possible mechanism of the amelioration of EAM by IL-10-Ig treatment.
References
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A protein kinase involved in the regulation of inflammatory cytokine biosynthesis.
Joseph C. Lee,Jeffrey T. Laydon,Peter C. McDonnell,Timothy Gallagher,Sanjay Kumar,David W. Green,Dean E. McNulty,M. J. Blumenthal,J. R. Heys,S. W. Landvatter,James E. Strickler,Megan M. McLaughlin,I. R. Siemens,Seth M. Fisher,George P. Livi,John R. White,Jerry L. Adams,Peter Young +17 more
TL;DR: Production of interleukin-1 and tumour necrosis factor from stimulated human monocytes is inhibited by a new series of pyridinyl-imidazole compounds, suggesting that the CSBPs are critical for cytokine production.
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Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF.
TL;DR: The results suggest that binding and/or phagocytosis of apoptotic cells induces active antiinflammatory or suppressive properties in human macrophages, likely that resolution of inflammation depends not only on the removal of apoptosis but on active suppression of inflammatory mediator production.
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Modulation of osteoclast differentiation and function by the new members of the tumor necrosis factor receptor and ligand families.
TL;DR: Osteoblasts/stromal cells can now be replaced with RANKL and M-CSF in dealing with the whole life of osteoclasts, and new ways to treat several metabolic bone diseases caused by abnormal osteoclast recruitment and functions will be established.
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Resolution of inflammation: the beginning programs the end.
Charles N. Serhan,John Savill +1 more
TL;DR: Emerging evidence now suggests that an active, coordinated program of resolution initiates in the first few hours after an inflammatory response begins, and the mechanism required for inflammation resolution may underpin the development of drugs that can resolve inflammatory processes in directed and controlled ways.
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Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand
Young-Yun Kong,Ulrich Feige,Iidiko Sarosi,Brad Bolon,Anna Tafuri,Sean Morony,Casey Capparelli,Ji Li,Robin Elliott,Susan McCabe,Tom Wong,G Campagnuolo,Erika Moran,Earl R. Bogoch,Gwyneth Van,Linh T. Nguyen,Pamela S. Ohashi,David L. Lacey,Eleanor N. Fish,William J. Boyle,Josef M. Penninger,Josef M. Penninger +21 more
TL;DR: The results show that both systemic and local T-cell activation can lead to OPGL production and subsequent bone loss, and they provide a novel paradigm for T cells as regulators of bone physiology.