Methyl palmitate inhibits lipopolysaccharide-stimulated phagocytic activity of rat peritoneal macrophages

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Macrophages, in general, are critical effectors of body's immune system. Chemical inhibition of phagocytic activity of such macrophages as Kupffer cells has been extensively studied. We have earlier shown that methyl palmitate (MP) inhibits the activation of Kupffer cells. To evaluate the potential of MP to inhibit the activation of other macrophages, we treated rat peritoneal macrophages with varying concentrations of MP. Its treatment led to a dose-dependent inhibition of phagocytic activity, which was found to be 34%, 47%, and 66% at 0.25, 0.50, and 1.0 mM MP, respectively, as measured by latex bead uptake. When MP-treated peritoneal macrophages were stimulated with lipopolysaccharide (LPS), the nitric oxide ONO) release was inhibited at 6 h, while cyclooxygenase-2 expression decreased after 24 h. The treatment with MP increased the release of interleukin (IL)-10 in the LPS-treated cells at 6 h, while IL-6 and tumor necrosis factor-α were significantly increased both at 6 and 24 h. Our data suggest that MP inhibits phagocytic activity and .NO production similar to that observed in isolated Kupffer cells. Therefore, inhibition of phagocytosis by MP may be a general phenomenon, and it could be used as an inhibitor of macrophage function.

Original languageEnglish (US)
Pages (from-to)302-308
Number of pages7
JournalJournal of Biochemical and Molecular Toxicology
Volume20
Issue number6
DOIs
StatePublished - 2006

Fingerprint

Macrophages
Peritoneal Macrophages
Lipopolysaccharides
Rats
Kupffer Cells
Chemical activation
Macrophage Activation
methyl palmitate
Immune system
Latex
Cyclooxygenase 2
Microspheres
Phagocytosis
Interleukin-10
Immune System
Interleukin-6
Nitric Oxide
Tumor Necrosis Factor-alpha
Cells

Keywords

  • Methyl Palmitate
  • Peritoneal Macrophages
  • Phagocytosis

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

@article{10962b6488084e0fb4b918a510b66395,
title = "Methyl palmitate inhibits lipopolysaccharide-stimulated phagocytic activity of rat peritoneal macrophages",
abstract = "Macrophages, in general, are critical effectors of body's immune system. Chemical inhibition of phagocytic activity of such macrophages as Kupffer cells has been extensively studied. We have earlier shown that methyl palmitate (MP) inhibits the activation of Kupffer cells. To evaluate the potential of MP to inhibit the activation of other macrophages, we treated rat peritoneal macrophages with varying concentrations of MP. Its treatment led to a dose-dependent inhibition of phagocytic activity, which was found to be 34{\%}, 47{\%}, and 66{\%} at 0.25, 0.50, and 1.0 mM MP, respectively, as measured by latex bead uptake. When MP-treated peritoneal macrophages were stimulated with lipopolysaccharide (LPS), the nitric oxide ONO) release was inhibited at 6 h, while cyclooxygenase-2 expression decreased after 24 h. The treatment with MP increased the release of interleukin (IL)-10 in the LPS-treated cells at 6 h, while IL-6 and tumor necrosis factor-α were significantly increased both at 6 and 24 h. Our data suggest that MP inhibits phagocytic activity and .NO production similar to that observed in isolated Kupffer cells. Therefore, inhibition of phagocytosis by MP may be a general phenomenon, and it could be used as an inhibitor of macrophage function.",
keywords = "Methyl Palmitate, Peritoneal Macrophages, Phagocytosis",
author = "Swapna Sarkar and M Khan and Bhupendra Kaphalia and Ghulam Ansari",
year = "2006",
doi = "10.1002/jbt.20150",
language = "English (US)",
volume = "20",
pages = "302--308",
journal = "Journal of Biochemical and Molecular Toxicology",
issn = "1095-6670",
publisher = "John Wiley and Sons Inc.",
number = "6",

}

TY - JOUR

T1 - Methyl palmitate inhibits lipopolysaccharide-stimulated phagocytic activity of rat peritoneal macrophages

AU - Sarkar, Swapna

AU - Khan, M

AU - Kaphalia, Bhupendra

AU - Ansari, Ghulam

PY - 2006

Y1 - 2006

N2 - Macrophages, in general, are critical effectors of body's immune system. Chemical inhibition of phagocytic activity of such macrophages as Kupffer cells has been extensively studied. We have earlier shown that methyl palmitate (MP) inhibits the activation of Kupffer cells. To evaluate the potential of MP to inhibit the activation of other macrophages, we treated rat peritoneal macrophages with varying concentrations of MP. Its treatment led to a dose-dependent inhibition of phagocytic activity, which was found to be 34%, 47%, and 66% at 0.25, 0.50, and 1.0 mM MP, respectively, as measured by latex bead uptake. When MP-treated peritoneal macrophages were stimulated with lipopolysaccharide (LPS), the nitric oxide ONO) release was inhibited at 6 h, while cyclooxygenase-2 expression decreased after 24 h. The treatment with MP increased the release of interleukin (IL)-10 in the LPS-treated cells at 6 h, while IL-6 and tumor necrosis factor-α were significantly increased both at 6 and 24 h. Our data suggest that MP inhibits phagocytic activity and .NO production similar to that observed in isolated Kupffer cells. Therefore, inhibition of phagocytosis by MP may be a general phenomenon, and it could be used as an inhibitor of macrophage function.

AB - Macrophages, in general, are critical effectors of body's immune system. Chemical inhibition of phagocytic activity of such macrophages as Kupffer cells has been extensively studied. We have earlier shown that methyl palmitate (MP) inhibits the activation of Kupffer cells. To evaluate the potential of MP to inhibit the activation of other macrophages, we treated rat peritoneal macrophages with varying concentrations of MP. Its treatment led to a dose-dependent inhibition of phagocytic activity, which was found to be 34%, 47%, and 66% at 0.25, 0.50, and 1.0 mM MP, respectively, as measured by latex bead uptake. When MP-treated peritoneal macrophages were stimulated with lipopolysaccharide (LPS), the nitric oxide ONO) release was inhibited at 6 h, while cyclooxygenase-2 expression decreased after 24 h. The treatment with MP increased the release of interleukin (IL)-10 in the LPS-treated cells at 6 h, while IL-6 and tumor necrosis factor-α were significantly increased both at 6 and 24 h. Our data suggest that MP inhibits phagocytic activity and .NO production similar to that observed in isolated Kupffer cells. Therefore, inhibition of phagocytosis by MP may be a general phenomenon, and it could be used as an inhibitor of macrophage function.

KW - Methyl Palmitate

KW - Peritoneal Macrophages

KW - Phagocytosis

UR - http://www.scopus.com/inward/record.url?scp=33845884313&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33845884313&partnerID=8YFLogxK

U2 - 10.1002/jbt.20150

DO - 10.1002/jbt.20150

M3 - Article

VL - 20

SP - 302

EP - 308

JO - Journal of Biochemical and Molecular Toxicology

JF - Journal of Biochemical and Molecular Toxicology

SN - 1095-6670

IS - 6

ER -