Phosphatidylserine-containing liposomes: Potential pharmacological interventions against inflammatory and immune diseases through the production of prostaglandin E2 after uptake by myeloid derived phagocytes

Hiro Take, Hiroshi Nakanishi

研究成果: ジャーナルへの寄稿評論記事

17 引用 (Scopus)

抄録

Phosphatidylserine (PS), which is normally located on the inner leaflet of the plasma membrane, translocates to the outer leaflet at the early stage of apoptosis. The PS externalization provides a signal for phagocytes to initiate uptake of apoptotic cells. After phagocytosis of apoptotic cells, phagocytes induce the secretion of anti-inflammatory mediators including prostaglandin E2 (PGE2). PS-containing liposomes (PSLs) can mimic the effects of apoptotic cells on phagocytes to induce the secretion of PGE 2. PSLs induce the PGE2 secretion from microglia without induction of either cyclooxygenase (COX)-2 or microsomal prostaglandin E synthase (mPGES)-1. PSLs are found to rather utilize COX-1/mPGES-2 system to produce PGE2 secretion and then shift microglia and macrophages from pro- to anti-inflammatory phenotype by an autocrine action of PGE2. Moreover, PSLs inhibit the maturation of dendritic cells and osteoclast precursors. Therefore, PSLs will be potential pharmacological interventions for inflammatory and immune diseases through feedback mechanism utilizing PGE 2.

元の言語英語
ページ(範囲)195-201
ページ数7
ジャーナルArchivum Immunologiae et Therapiae Experimentalis
59
発行部数3
DOI
出版物ステータス出版済み - 6 1 2011

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Phosphatidylserines
Immune System Diseases
Phagocytes
Dinoprostone
Liposomes
Pharmacology
Microglia
Prostaglandins E
Anti-Inflammatory Agents
Cytophagocytosis
Cyclooxygenase 1
Osteoclasts
Cyclooxygenase 2
Dendritic Cells
Macrophages
Cell Membrane
Apoptosis
Phenotype
Prostaglandin-E Synthases

All Science Journal Classification (ASJC) codes

  • Immunology
  • Immunology and Allergy

これを引用

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title = "Phosphatidylserine-containing liposomes: Potential pharmacological interventions against inflammatory and immune diseases through the production of prostaglandin E2 after uptake by myeloid derived phagocytes",
abstract = "Phosphatidylserine (PS), which is normally located on the inner leaflet of the plasma membrane, translocates to the outer leaflet at the early stage of apoptosis. The PS externalization provides a signal for phagocytes to initiate uptake of apoptotic cells. After phagocytosis of apoptotic cells, phagocytes induce the secretion of anti-inflammatory mediators including prostaglandin E2 (PGE2). PS-containing liposomes (PSLs) can mimic the effects of apoptotic cells on phagocytes to induce the secretion of PGE 2. PSLs induce the PGE2 secretion from microglia without induction of either cyclooxygenase (COX)-2 or microsomal prostaglandin E synthase (mPGES)-1. PSLs are found to rather utilize COX-1/mPGES-2 system to produce PGE2 secretion and then shift microglia and macrophages from pro- to anti-inflammatory phenotype by an autocrine action of PGE2. Moreover, PSLs inhibit the maturation of dendritic cells and osteoclast precursors. Therefore, PSLs will be potential pharmacological interventions for inflammatory and immune diseases through feedback mechanism utilizing PGE 2.",
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T2 - Potential pharmacological interventions against inflammatory and immune diseases through the production of prostaglandin E2 after uptake by myeloid derived phagocytes

AU - Take, Hiro

AU - Nakanishi, Hiroshi

PY - 2011/6/1

Y1 - 2011/6/1

N2 - Phosphatidylserine (PS), which is normally located on the inner leaflet of the plasma membrane, translocates to the outer leaflet at the early stage of apoptosis. The PS externalization provides a signal for phagocytes to initiate uptake of apoptotic cells. After phagocytosis of apoptotic cells, phagocytes induce the secretion of anti-inflammatory mediators including prostaglandin E2 (PGE2). PS-containing liposomes (PSLs) can mimic the effects of apoptotic cells on phagocytes to induce the secretion of PGE 2. PSLs induce the PGE2 secretion from microglia without induction of either cyclooxygenase (COX)-2 or microsomal prostaglandin E synthase (mPGES)-1. PSLs are found to rather utilize COX-1/mPGES-2 system to produce PGE2 secretion and then shift microglia and macrophages from pro- to anti-inflammatory phenotype by an autocrine action of PGE2. Moreover, PSLs inhibit the maturation of dendritic cells and osteoclast precursors. Therefore, PSLs will be potential pharmacological interventions for inflammatory and immune diseases through feedback mechanism utilizing PGE 2.

AB - Phosphatidylserine (PS), which is normally located on the inner leaflet of the plasma membrane, translocates to the outer leaflet at the early stage of apoptosis. The PS externalization provides a signal for phagocytes to initiate uptake of apoptotic cells. After phagocytosis of apoptotic cells, phagocytes induce the secretion of anti-inflammatory mediators including prostaglandin E2 (PGE2). PS-containing liposomes (PSLs) can mimic the effects of apoptotic cells on phagocytes to induce the secretion of PGE 2. PSLs induce the PGE2 secretion from microglia without induction of either cyclooxygenase (COX)-2 or microsomal prostaglandin E synthase (mPGES)-1. PSLs are found to rather utilize COX-1/mPGES-2 system to produce PGE2 secretion and then shift microglia and macrophages from pro- to anti-inflammatory phenotype by an autocrine action of PGE2. Moreover, PSLs inhibit the maturation of dendritic cells and osteoclast precursors. Therefore, PSLs will be potential pharmacological interventions for inflammatory and immune diseases through feedback mechanism utilizing PGE 2.

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