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Open AccessJournal ArticleDOI

Phosphatidylserine-containing liposomes suppress inflammatory bone loss by ameliorating the cytokine imbalance provoked by infiltrated macrophages.

Hong Mei Ma, +2 more
- 01 Jun 2011 - 
- Vol. 91, Iss: 6, pp 921-931
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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.

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Citations
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Journal ArticleDOI

Pathways for Bone Loss in Inflammatory Disease

TL;DR: This review summarizes new data on inflammatory bone loss obtained in 2011 and describes the molecular pathways by which receptor activator of nuclear factor-κB ligand and RANKL induce osteoclast differentiation.
Journal ArticleDOI

HCMV reprogramming of infected monocyte survival and differentiation: a Goldilocks phenomenon.

TL;DR: The induction of a uniquely polarized macrophage subset from infected monocytes is described, which is argued to be the ideal cellular environment for the initiation of viral gene expression and replication and, ultimately, viral spread and persistence within the infected host.
Journal ArticleDOI

Myelin alters the inflammatory phenotype of macrophages by activating PPARs

TL;DR: The data show that myelin modulates the phenotype of macrophages by PPAR activation, which may subsequently dampen MS lesion progression and the immunoregulatory impact of naturally-occurring myelin lipids may hold promise for future MS therapeutics.
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Anti-obesity and anti-inflammatory effects of macrophage-targeted interleukin-10-conjugated liposomes in obese mice.

TL;DR: The findings suggest that the PSL-IL10 has macrophage targeting ability and enhanced anti- inflammatory effect due to the synergistic anti-inflammatory effects of IL-10 and PSL, and can be used as amacrophage-targeted therapeutic material for inflammation-related diseases, including obesity.
References
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Journal ArticleDOI

Synovial tissue in rheumatoid arthritis is a source of osteoclast differentiation factor

TL;DR: These studies address the potential role of ODF and the bone and marrow microenvironment in the pathogenesis of osteoclast-mediated bone erosion in RA and identify TRAP-positive, cathepsin K-positive osteOClast precursor cells are identified in areas of pannus invasion into bone in RA.
Journal ArticleDOI

Phosphatidylserine (PS) induces PS receptor–mediated macropinocytosis and promotes clearance of apoptotic cells

TL;DR: The results suggest that regardless of the receptors engaged on the phagocyte, ingestion does not occur in the absence of phosphatidylserine (PS), and recognition of PS was found to be dependent on the presence of the PS receptor (PSR).
Journal Article

Extracellular signal-related kinase (ERK) and p38 mitogen-activated protein (MAP) kinases differentially regulate the lipopolysaccharide-mediated induction of inducible nitric oxide synthase and IL-12 in macrophages: Leishmania phosphoglycans subvert macrophage IL-12 production by targeting ERK MAP kinase

TL;DR: As ERK and p38 MAP kinases differentially regulate the induction of the macrophage effector molecules, inducible NO synthase and IL-12, these kinases are potential targets not only for the development of novel strategies to combat intracellular pathogens but also for therapeutic immunomodulation.
Journal ArticleDOI

Critical roles for interleukin 1 and tumor necrosis factor alpha in antibody-induced arthritis

TL;DR: It was found that all mice with strong inflammation exhibited the bone erosion and reconstruction phenomena typical of K/BxN arthritis, with no evidence of any particular requirement for TNFα for bone destruction.
Journal ArticleDOI

Signalling, inflammation and arthritis NF-κB and its relevance to arthritis and inflammation

TL;DR: The importance of NF-kappaB in inflammation is undisputed and inhibition of the pathway is widely believed to have great potential as a therapeutic target in RA, but it will be important that such inhibitors are carefully monitored before their long-term use in chronic inflammatory conditions such as RA.
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