Macrophage Polarization and Activation in Response to Implant Debris: Influence by "Particle Disease" and "Ion Disease

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F14%3A33153041" target="_blank" >RIV/61989592:15110/14:33153041 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1615/JLongTermEffMedImplants.2014011355" target="_blank" >http://dx.doi.org/10.1615/JLongTermEffMedImplants.2014011355</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1615/JLongTermEffMedImplants.2014011355" target="_blank" >10.1615/JLongTermEffMedImplants.2014011355</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Macrophage Polarization and Activation in Response to Implant Debris: Influence by "Particle Disease" and "Ion Disease

Popis výsledku v původním jazyce

Macrophages derive from human embryonic and fetal stem cells and from human bone marrow-derived blood monocytes. They play a major homeostatic role in tissue remodeling and maintenance facilitated by apoptotic "eat me" opsonins like CRP, serum amyloid P,C1q, C3b, IgM, ficolin, and surfactant proteins. Three subsets of monocytes, classic, intermediate, and nonclassic, are mobilized and transmigrate to tissues. Implant-derived wear particles opsonized by danger signals regulate macrophage priming, polarization (M1, M2, M17, and Mreg), and activation. CD14+ monocytes in healthy controls and CD16+ monocytes in inflammation differentiate/polarize to foreign body giant cells/osteoclasts or inflammatory dendritic cells (infDC). These danger signal opsonins can be pathogen- or microbe-associated molecular patterns (PAMPs/MAMPs), but in aseptic loosening, usually are damage-associated molecular patterns (DAMPs). Danger signal-opsonized particles elicit "particle disease" and aseptic loosening.

Název v anglickém jazyce

Macrophage Polarization and Activation in Response to Implant Debris: Influence by "Particle Disease" and "Ion Disease

Popis výsledku anglicky

Macrophages derive from human embryonic and fetal stem cells and from human bone marrow-derived blood monocytes. They play a major homeostatic role in tissue remodeling and maintenance facilitated by apoptotic "eat me" opsonins like CRP, serum amyloid P,C1q, C3b, IgM, ficolin, and surfactant proteins. Three subsets of monocytes, classic, intermediate, and nonclassic, are mobilized and transmigrate to tissues. Implant-derived wear particles opsonized by danger signals regulate macrophage priming, polarization (M1, M2, M17, and Mreg), and activation. CD14+ monocytes in healthy controls and CD16+ monocytes in inflammation differentiate/polarize to foreign body giant cells/osteoclasts or inflammatory dendritic cells (infDC). These danger signal opsonins can be pathogen- or microbe-associated molecular patterns (PAMPs/MAMPs), but in aseptic loosening, usually are damage-associated molecular patterns (DAMPs). Danger signal-opsonized particles elicit "particle disease" and aseptic loosening.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FI - Traumatologie a ortopedie

OECD FORD obor

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Projekt

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Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2014

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Long-Term Effects of Medical Implants

ISSN

1050-6934

e-ISSN

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Svazek periodika

24

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

15

Strana od-do

267-281

Kód UT WoS článku

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EID výsledku v databázi Scopus

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