Contribution of Kupffer cells to liposome accumulation in the liver

Emma Samuelsson, Haifa Shen, Elvin Blanco, Mauro Ferrari, Joy Wolfram

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The liver is a major barrier for site-specific delivery of systemically injected nanoparticles, as up to 90% of the dose is usually captured by this organ. Kupffer cells are thought to be the main cellular component responsible for nanoparticle accumulation in the liver. These resident macrophages form part of the mononuclear phagocyte system, which recognizes and engulfs foreign bodies in the circulatory system. In this study, we have compared two strategies for reducing nanoparticle accumulation in the liver, in order to investigate the specific contribution of Kupffer cells. Specifically, we have performed a comparison of the capability of pegylation and Kupffer cell depletion to reduce liposome accumulation in the liver. Pegylation reduces nanoparticle interactions with all types of cells and can serve as a control for elucidating the role of specific cell populations in liver accumulation. The results indicate that liposome pegylation is a more effective strategy for avoiding liver uptake compared to depletion of Kupffer cells, suggesting that nanoparticle interactions with other cells in the liver may also play a contributing role. This study highlights the need for a more complete understanding of factors that mediate nanoparticle accumulation in the liver and for the exploration of microenvironmental modulation strategies for reducing nanoparticle-cell interactions in this organ.

Original languageEnglish (US)
Pages (from-to)356-362
Number of pages7
JournalColloids and Surfaces B: Biointerfaces
Volume158
DOIs
StatePublished - Oct 1 2017

Fingerprint

Kupffer Cells
Liposomes
liver
Liver
Nanoparticles
nanoparticles
cells
organs
depletion
foreign bodies
circulatory system
Mononuclear Phagocyte System
macrophages
Macrophages
interactions
Cardiovascular System
Foreign Bodies
Cell Communication
delivery
Cells

Keywords

  • Kupffer cells
  • Liver
  • Macrophages
  • Mononuclear phagocyte system
  • Nanoparticles
  • Pegylation

ASJC Scopus subject areas

  • Biotechnology
  • Surfaces and Interfaces
  • Physical and Theoretical Chemistry
  • Colloid and Surface Chemistry

Cite this

Contribution of Kupffer cells to liposome accumulation in the liver. / Samuelsson, Emma; Shen, Haifa; Blanco, Elvin; Ferrari, Mauro; Wolfram, Joy.

In: Colloids and Surfaces B: Biointerfaces, Vol. 158, 01.10.2017, p. 356-362.

Research output: Contribution to journalArticle

Samuelsson, Emma ; Shen, Haifa ; Blanco, Elvin ; Ferrari, Mauro ; Wolfram, Joy. / Contribution of Kupffer cells to liposome accumulation in the liver. In: Colloids and Surfaces B: Biointerfaces. 2017 ; Vol. 158. pp. 356-362.
@article{688cc00ea65f48aa91de77d9f9a73443,
title = "Contribution of Kupffer cells to liposome accumulation in the liver",
abstract = "The liver is a major barrier for site-specific delivery of systemically injected nanoparticles, as up to 90{\%} of the dose is usually captured by this organ. Kupffer cells are thought to be the main cellular component responsible for nanoparticle accumulation in the liver. These resident macrophages form part of the mononuclear phagocyte system, which recognizes and engulfs foreign bodies in the circulatory system. In this study, we have compared two strategies for reducing nanoparticle accumulation in the liver, in order to investigate the specific contribution of Kupffer cells. Specifically, we have performed a comparison of the capability of pegylation and Kupffer cell depletion to reduce liposome accumulation in the liver. Pegylation reduces nanoparticle interactions with all types of cells and can serve as a control for elucidating the role of specific cell populations in liver accumulation. The results indicate that liposome pegylation is a more effective strategy for avoiding liver uptake compared to depletion of Kupffer cells, suggesting that nanoparticle interactions with other cells in the liver may also play a contributing role. This study highlights the need for a more complete understanding of factors that mediate nanoparticle accumulation in the liver and for the exploration of microenvironmental modulation strategies for reducing nanoparticle-cell interactions in this organ.",
keywords = "Kupffer cells, Liver, Macrophages, Mononuclear phagocyte system, Nanoparticles, Pegylation",
author = "Emma Samuelsson and Haifa Shen and Elvin Blanco and Mauro Ferrari and Joy Wolfram",
year = "2017",
month = "10",
day = "1",
doi = "10.1016/j.colsurfb.2017.07.014",
language = "English (US)",
volume = "158",
pages = "356--362",
journal = "Colloids and Surfaces B: Biointerfaces",
issn = "0927-7765",
publisher = "Elsevier",

}

TY - JOUR

T1 - Contribution of Kupffer cells to liposome accumulation in the liver

AU - Samuelsson, Emma

AU - Shen, Haifa

AU - Blanco, Elvin

AU - Ferrari, Mauro

AU - Wolfram, Joy

PY - 2017/10/1

Y1 - 2017/10/1

N2 - The liver is a major barrier for site-specific delivery of systemically injected nanoparticles, as up to 90% of the dose is usually captured by this organ. Kupffer cells are thought to be the main cellular component responsible for nanoparticle accumulation in the liver. These resident macrophages form part of the mononuclear phagocyte system, which recognizes and engulfs foreign bodies in the circulatory system. In this study, we have compared two strategies for reducing nanoparticle accumulation in the liver, in order to investigate the specific contribution of Kupffer cells. Specifically, we have performed a comparison of the capability of pegylation and Kupffer cell depletion to reduce liposome accumulation in the liver. Pegylation reduces nanoparticle interactions with all types of cells and can serve as a control for elucidating the role of specific cell populations in liver accumulation. The results indicate that liposome pegylation is a more effective strategy for avoiding liver uptake compared to depletion of Kupffer cells, suggesting that nanoparticle interactions with other cells in the liver may also play a contributing role. This study highlights the need for a more complete understanding of factors that mediate nanoparticle accumulation in the liver and for the exploration of microenvironmental modulation strategies for reducing nanoparticle-cell interactions in this organ.

AB - The liver is a major barrier for site-specific delivery of systemically injected nanoparticles, as up to 90% of the dose is usually captured by this organ. Kupffer cells are thought to be the main cellular component responsible for nanoparticle accumulation in the liver. These resident macrophages form part of the mononuclear phagocyte system, which recognizes and engulfs foreign bodies in the circulatory system. In this study, we have compared two strategies for reducing nanoparticle accumulation in the liver, in order to investigate the specific contribution of Kupffer cells. Specifically, we have performed a comparison of the capability of pegylation and Kupffer cell depletion to reduce liposome accumulation in the liver. Pegylation reduces nanoparticle interactions with all types of cells and can serve as a control for elucidating the role of specific cell populations in liver accumulation. The results indicate that liposome pegylation is a more effective strategy for avoiding liver uptake compared to depletion of Kupffer cells, suggesting that nanoparticle interactions with other cells in the liver may also play a contributing role. This study highlights the need for a more complete understanding of factors that mediate nanoparticle accumulation in the liver and for the exploration of microenvironmental modulation strategies for reducing nanoparticle-cell interactions in this organ.

KW - Kupffer cells

KW - Liver

KW - Macrophages

KW - Mononuclear phagocyte system

KW - Nanoparticles

KW - Pegylation

UR - http://www.scopus.com/inward/record.url?scp=85024099122&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85024099122&partnerID=8YFLogxK

U2 - 10.1016/j.colsurfb.2017.07.014

DO - 10.1016/j.colsurfb.2017.07.014

M3 - Article

VL - 158

SP - 356

EP - 362

JO - Colloids and Surfaces B: Biointerfaces

JF - Colloids and Surfaces B: Biointerfaces

SN - 0927-7765

ER -