Methyl palmitate

Inhibitor of phagocytosis in primary rat Kupffer cells

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Kupffer cells are involved in phagocytosis and known to release biologically active mediators during early events of liver injury. Such functional properties of Kupffer cells can be modulated by methyl palmitate (MP). Therefore, efficacy of MP to modulate Kupffer cell function was evaluated in cultured primary Kupffer cells from rat liver. Phagocytic activity of Kupffer cells was measured by their capacity to phagocytize latex beads and the release of TNF-α, IL-10, IL-6, nitric oxide, and PGE2 was determined in cell culture medium after incubating the cells with various concentrations of MP for 24 h followed stimulation with lipopolysaccharide (LPS) for 6 h. To understand the mechanism of phagocytosis, we investigated the hydrolysis of MP, and determine ATP levels and activity of NF-κB in MP-inhibited Kupffer cells. A significant decrease was observed in phagocytosis. Phagocytosis evaluated at 0.5 mM MP was found to be time-dependent with a maximum decrease of 49% at 6 h. Exposure of Kupffer cells to MP followed by LPS stimulation showed a dose-dependent decrease in phagocytosis and reduced the release of TNF-α, IL-10, nitric oxide, and PGE2 but not of IL-6 levels in the supernatant as compared to the control. While ATP levels were unchanged, the nuclear factor NF-κB (p65) activity was inhibited in Kupffer cells treated with MP after LPS stimulation (35.6 RLU versus 49.6 RLU in control). Hydrolysis of MP was found to be time-dependent; maximum concentration of MP and palmitic acid (hydrolysis products) in the cell being at 3 and 6 h, respectively. In general, MP appears to reduce phagocytosis and levels of TNF-α, IL-10, nitric oxide, and PGE2 without affecting ATP levels and is probably mediated by NF-κB. This in vitro model is useful for detailed mechanistic studies of inhibition of phagocytosis by MP and other fatty acid esters.

Original languageEnglish (US)
Pages (from-to)197-204
Number of pages8
JournalToxicology
Volume210
Issue number2-3
DOIs
StatePublished - Jun 1 2005

Fingerprint

Kupffer Cells
Phagocytosis
Rats
Dinoprostone
Interleukin-10
Lipopolysaccharides
Hydrolysis
Nitric Oxide
Adenosine Triphosphate
Liver
methyl palmitate
Interleukin-6
Palmitic Acid
Latex
Microspheres
Cell culture
Culture Media
Esters
Fatty Acids
Cell Culture Techniques

Keywords

  • Kupffer cell
  • Methyl palmitate
  • NF-κB
  • Phagocytosis

ASJC Scopus subject areas

  • Toxicology

Cite this

Methyl palmitate : Inhibitor of phagocytosis in primary rat Kupffer cells. / Cai, P.; Kaphalia, Bhupendra; Ansari, Ghulam.

In: Toxicology, Vol. 210, No. 2-3, 01.06.2005, p. 197-204.

Research output: Contribution to journalArticle

@article{b8db9bd5b9fd4c1991d8032902d023f5,
title = "Methyl palmitate: Inhibitor of phagocytosis in primary rat Kupffer cells",
abstract = "Kupffer cells are involved in phagocytosis and known to release biologically active mediators during early events of liver injury. Such functional properties of Kupffer cells can be modulated by methyl palmitate (MP). Therefore, efficacy of MP to modulate Kupffer cell function was evaluated in cultured primary Kupffer cells from rat liver. Phagocytic activity of Kupffer cells was measured by their capacity to phagocytize latex beads and the release of TNF-α, IL-10, IL-6, nitric oxide, and PGE2 was determined in cell culture medium after incubating the cells with various concentrations of MP for 24 h followed stimulation with lipopolysaccharide (LPS) for 6 h. To understand the mechanism of phagocytosis, we investigated the hydrolysis of MP, and determine ATP levels and activity of NF-κB in MP-inhibited Kupffer cells. A significant decrease was observed in phagocytosis. Phagocytosis evaluated at 0.5 mM MP was found to be time-dependent with a maximum decrease of 49{\%} at 6 h. Exposure of Kupffer cells to MP followed by LPS stimulation showed a dose-dependent decrease in phagocytosis and reduced the release of TNF-α, IL-10, nitric oxide, and PGE2 but not of IL-6 levels in the supernatant as compared to the control. While ATP levels were unchanged, the nuclear factor NF-κB (p65) activity was inhibited in Kupffer cells treated with MP after LPS stimulation (35.6 RLU versus 49.6 RLU in control). Hydrolysis of MP was found to be time-dependent; maximum concentration of MP and palmitic acid (hydrolysis products) in the cell being at 3 and 6 h, respectively. In general, MP appears to reduce phagocytosis and levels of TNF-α, IL-10, nitric oxide, and PGE2 without affecting ATP levels and is probably mediated by NF-κB. This in vitro model is useful for detailed mechanistic studies of inhibition of phagocytosis by MP and other fatty acid esters.",
keywords = "Kupffer cell, Methyl palmitate, NF-κB, Phagocytosis",
author = "P. Cai and Bhupendra Kaphalia and Ghulam Ansari",
year = "2005",
month = "6",
day = "1",
doi = "10.1016/j.tox.2005.02.001",
language = "English (US)",
volume = "210",
pages = "197--204",
journal = "Toxicology",
issn = "0300-483X",
publisher = "Elsevier Ireland Ltd",
number = "2-3",

}

TY - JOUR

T1 - Methyl palmitate

T2 - Inhibitor of phagocytosis in primary rat Kupffer cells

AU - Cai, P.

AU - Kaphalia, Bhupendra

AU - Ansari, Ghulam

PY - 2005/6/1

Y1 - 2005/6/1

N2 - Kupffer cells are involved in phagocytosis and known to release biologically active mediators during early events of liver injury. Such functional properties of Kupffer cells can be modulated by methyl palmitate (MP). Therefore, efficacy of MP to modulate Kupffer cell function was evaluated in cultured primary Kupffer cells from rat liver. Phagocytic activity of Kupffer cells was measured by their capacity to phagocytize latex beads and the release of TNF-α, IL-10, IL-6, nitric oxide, and PGE2 was determined in cell culture medium after incubating the cells with various concentrations of MP for 24 h followed stimulation with lipopolysaccharide (LPS) for 6 h. To understand the mechanism of phagocytosis, we investigated the hydrolysis of MP, and determine ATP levels and activity of NF-κB in MP-inhibited Kupffer cells. A significant decrease was observed in phagocytosis. Phagocytosis evaluated at 0.5 mM MP was found to be time-dependent with a maximum decrease of 49% at 6 h. Exposure of Kupffer cells to MP followed by LPS stimulation showed a dose-dependent decrease in phagocytosis and reduced the release of TNF-α, IL-10, nitric oxide, and PGE2 but not of IL-6 levels in the supernatant as compared to the control. While ATP levels were unchanged, the nuclear factor NF-κB (p65) activity was inhibited in Kupffer cells treated with MP after LPS stimulation (35.6 RLU versus 49.6 RLU in control). Hydrolysis of MP was found to be time-dependent; maximum concentration of MP and palmitic acid (hydrolysis products) in the cell being at 3 and 6 h, respectively. In general, MP appears to reduce phagocytosis and levels of TNF-α, IL-10, nitric oxide, and PGE2 without affecting ATP levels and is probably mediated by NF-κB. This in vitro model is useful for detailed mechanistic studies of inhibition of phagocytosis by MP and other fatty acid esters.

AB - Kupffer cells are involved in phagocytosis and known to release biologically active mediators during early events of liver injury. Such functional properties of Kupffer cells can be modulated by methyl palmitate (MP). Therefore, efficacy of MP to modulate Kupffer cell function was evaluated in cultured primary Kupffer cells from rat liver. Phagocytic activity of Kupffer cells was measured by their capacity to phagocytize latex beads and the release of TNF-α, IL-10, IL-6, nitric oxide, and PGE2 was determined in cell culture medium after incubating the cells with various concentrations of MP for 24 h followed stimulation with lipopolysaccharide (LPS) for 6 h. To understand the mechanism of phagocytosis, we investigated the hydrolysis of MP, and determine ATP levels and activity of NF-κB in MP-inhibited Kupffer cells. A significant decrease was observed in phagocytosis. Phagocytosis evaluated at 0.5 mM MP was found to be time-dependent with a maximum decrease of 49% at 6 h. Exposure of Kupffer cells to MP followed by LPS stimulation showed a dose-dependent decrease in phagocytosis and reduced the release of TNF-α, IL-10, nitric oxide, and PGE2 but not of IL-6 levels in the supernatant as compared to the control. While ATP levels were unchanged, the nuclear factor NF-κB (p65) activity was inhibited in Kupffer cells treated with MP after LPS stimulation (35.6 RLU versus 49.6 RLU in control). Hydrolysis of MP was found to be time-dependent; maximum concentration of MP and palmitic acid (hydrolysis products) in the cell being at 3 and 6 h, respectively. In general, MP appears to reduce phagocytosis and levels of TNF-α, IL-10, nitric oxide, and PGE2 without affecting ATP levels and is probably mediated by NF-κB. This in vitro model is useful for detailed mechanistic studies of inhibition of phagocytosis by MP and other fatty acid esters.

KW - Kupffer cell

KW - Methyl palmitate

KW - NF-κB

KW - Phagocytosis

UR - http://www.scopus.com/inward/record.url?scp=17144416472&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=17144416472&partnerID=8YFLogxK

U2 - 10.1016/j.tox.2005.02.001

DO - 10.1016/j.tox.2005.02.001

M3 - Article

VL - 210

SP - 197

EP - 204

JO - Toxicology

JF - Toxicology

SN - 0300-483X

IS - 2-3

ER -