Vespa tropica venom suppresses lipopolysaccharide-mediated secretion of pro-inflammatory cyto-chemokines by abrogating nuclear factor-κ B activation in microglia

Deepak Kumar Kaushik, Menaka Thounaojam, Arinjay Mitra, Anirban Basu

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Objective and design: The present study was aimed to evaluate the anti-inflammatory potentials of Vespa tropica (VT) venom and its isolated peptides. Effects of whole venom and its two peptides (Vt1512 and Vt1386) on lipopolysaccharide (LPS) challenged BV-2 murine microglial cells was evaluated. Materials: Mouse microglial cell line, BV-2 and crude venom extract as well as purified peptides from VT along with LPS from Salmonella enterica were used for the studies. Treatment: BV-2 cells were treated with 500 ng/ml of LPS and different doses of crude wasp venom as well as purified peptides. Methods: We used immunoblotting, cytokine bead arrays and fluorescence activated cell sorter (FACS) to evaluate the levels of various proteins, cytokines and reactive oxygen species (ROS). Results: Our studies suggest that treatment with whole venom significantly reduces oxidative stress and LPS-stimulated activation of microglia. Also, purified peptides from crude venom exhibited potential anti-inflammatory properties. Further, whole venom was found to be targeting Akt and p38 MAPK pathways, leading to suppressed NF-κB phosphorylation in LPS challenged BV-2 cells. Conclusions: VT venom possesses anti-inflammatory properties and can be further explored for their therapeutic potential in treating various inflammatory conditions of the central nervous system (CNS).

Original languageEnglish (US)
Pages (from-to)657-665
Number of pages9
JournalInflammation Research
Volume63
Issue number8
DOIs
StatePublished - Jan 1 2014
Externally publishedYes

Fingerprint

Wasp Venoms
Venoms
Microglia
Chemokines
Lipopolysaccharides
Peptides
Anti-Inflammatory Agents
Cytokines
Salmonella enterica
p38 Mitogen-Activated Protein Kinases
Complex Mixtures
Immunoblotting
Reactive Oxygen Species
Oxidative Stress
Central Nervous System
Fluorescence
Phosphorylation
Cell Line
Proteins

Keywords

  • Cytokines
  • Lipopolysaccharide
  • Microglia
  • Neuroinflammation
  • Wasp venom

ASJC Scopus subject areas

  • Immunology
  • Pharmacology

Cite this

Vespa tropica venom suppresses lipopolysaccharide-mediated secretion of pro-inflammatory cyto-chemokines by abrogating nuclear factor-κ B activation in microglia. / Kaushik, Deepak Kumar; Thounaojam, Menaka; Mitra, Arinjay; Basu, Anirban.

In: Inflammation Research, Vol. 63, No. 8, 01.01.2014, p. 657-665.

Research output: Contribution to journalArticle

@article{eee057e860ba47ffb31e5e9380286fdd,
title = "Vespa tropica venom suppresses lipopolysaccharide-mediated secretion of pro-inflammatory cyto-chemokines by abrogating nuclear factor-κ B activation in microglia",
abstract = "Objective and design: The present study was aimed to evaluate the anti-inflammatory potentials of Vespa tropica (VT) venom and its isolated peptides. Effects of whole venom and its two peptides (Vt1512 and Vt1386) on lipopolysaccharide (LPS) challenged BV-2 murine microglial cells was evaluated. Materials: Mouse microglial cell line, BV-2 and crude venom extract as well as purified peptides from VT along with LPS from Salmonella enterica were used for the studies. Treatment: BV-2 cells were treated with 500 ng/ml of LPS and different doses of crude wasp venom as well as purified peptides. Methods: We used immunoblotting, cytokine bead arrays and fluorescence activated cell sorter (FACS) to evaluate the levels of various proteins, cytokines and reactive oxygen species (ROS). Results: Our studies suggest that treatment with whole venom significantly reduces oxidative stress and LPS-stimulated activation of microglia. Also, purified peptides from crude venom exhibited potential anti-inflammatory properties. Further, whole venom was found to be targeting Akt and p38 MAPK pathways, leading to suppressed NF-κB phosphorylation in LPS challenged BV-2 cells. Conclusions: VT venom possesses anti-inflammatory properties and can be further explored for their therapeutic potential in treating various inflammatory conditions of the central nervous system (CNS).",
keywords = "Cytokines, Lipopolysaccharide, Microglia, Neuroinflammation, Wasp venom",
author = "Kaushik, {Deepak Kumar} and Menaka Thounaojam and Arinjay Mitra and Anirban Basu",
year = "2014",
month = "1",
day = "1",
doi = "10.1007/s00011-014-0738-0",
language = "English (US)",
volume = "63",
pages = "657--665",
journal = "Inflammation Research",
issn = "1023-3830",
publisher = "Birkhauser Verlag Basel",
number = "8",

}

TY - JOUR

T1 - Vespa tropica venom suppresses lipopolysaccharide-mediated secretion of pro-inflammatory cyto-chemokines by abrogating nuclear factor-κ B activation in microglia

AU - Kaushik, Deepak Kumar

AU - Thounaojam, Menaka

AU - Mitra, Arinjay

AU - Basu, Anirban

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Objective and design: The present study was aimed to evaluate the anti-inflammatory potentials of Vespa tropica (VT) venom and its isolated peptides. Effects of whole venom and its two peptides (Vt1512 and Vt1386) on lipopolysaccharide (LPS) challenged BV-2 murine microglial cells was evaluated. Materials: Mouse microglial cell line, BV-2 and crude venom extract as well as purified peptides from VT along with LPS from Salmonella enterica were used for the studies. Treatment: BV-2 cells were treated with 500 ng/ml of LPS and different doses of crude wasp venom as well as purified peptides. Methods: We used immunoblotting, cytokine bead arrays and fluorescence activated cell sorter (FACS) to evaluate the levels of various proteins, cytokines and reactive oxygen species (ROS). Results: Our studies suggest that treatment with whole venom significantly reduces oxidative stress and LPS-stimulated activation of microglia. Also, purified peptides from crude venom exhibited potential anti-inflammatory properties. Further, whole venom was found to be targeting Akt and p38 MAPK pathways, leading to suppressed NF-κB phosphorylation in LPS challenged BV-2 cells. Conclusions: VT venom possesses anti-inflammatory properties and can be further explored for their therapeutic potential in treating various inflammatory conditions of the central nervous system (CNS).

AB - Objective and design: The present study was aimed to evaluate the anti-inflammatory potentials of Vespa tropica (VT) venom and its isolated peptides. Effects of whole venom and its two peptides (Vt1512 and Vt1386) on lipopolysaccharide (LPS) challenged BV-2 murine microglial cells was evaluated. Materials: Mouse microglial cell line, BV-2 and crude venom extract as well as purified peptides from VT along with LPS from Salmonella enterica were used for the studies. Treatment: BV-2 cells were treated with 500 ng/ml of LPS and different doses of crude wasp venom as well as purified peptides. Methods: We used immunoblotting, cytokine bead arrays and fluorescence activated cell sorter (FACS) to evaluate the levels of various proteins, cytokines and reactive oxygen species (ROS). Results: Our studies suggest that treatment with whole venom significantly reduces oxidative stress and LPS-stimulated activation of microglia. Also, purified peptides from crude venom exhibited potential anti-inflammatory properties. Further, whole venom was found to be targeting Akt and p38 MAPK pathways, leading to suppressed NF-κB phosphorylation in LPS challenged BV-2 cells. Conclusions: VT venom possesses anti-inflammatory properties and can be further explored for their therapeutic potential in treating various inflammatory conditions of the central nervous system (CNS).

KW - Cytokines

KW - Lipopolysaccharide

KW - Microglia

KW - Neuroinflammation

KW - Wasp venom

UR - http://www.scopus.com/inward/record.url?scp=84904321436&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84904321436&partnerID=8YFLogxK

U2 - 10.1007/s00011-014-0738-0

DO - 10.1007/s00011-014-0738-0

M3 - Article

C2 - 24781802

AN - SCOPUS:84904321436

VL - 63

SP - 657

EP - 665

JO - Inflammation Research

JF - Inflammation Research

SN - 1023-3830

IS - 8

ER -