Microglial cells and peritoneal macrophages release activin A upon stimulation with Toll-like receptor agonists

Sandra Ebert1, Moritz Zeretzke, Roland Nau

  • 1Department of Neurology, University of Göttingen, Robert-Koch-Street 40, 37075 Göttingen, Germany. sebert1@gwdg.de

Neuroscience Letters
|December 30, 2006
PubMed

Insights

Microglia and macrophages release activin A when immune receptors are activated. This suggests these cells are the source of elevated activin A in meningitis and sepsis.

Area of Science:

  • Immunology
  • Neuroscience
  • Cell Biology

Background:

  • Elevated activin A concentrations are observed in cerebrospinal fluid (CSF) during meningitis and in serum during sepsis.
  • The cellular sources of increased activin A in these conditions remain unidentified.

Purpose of the Study:

  • To investigate the cellular origin of elevated activin A in inflammatory conditions.
  • To determine if immune cells, specifically microglia and macrophages, produce activin A in response to immune stimuli.

Main Methods:

  • Primary mouse microglial cells and peritoneal macrophages were cultured.
  • Cells were treated with agonists for Toll-like receptors (TLRs) 2, 4, and 9.
  • Activin A release was measured following stimulation.

Main Results:

  • Microglial cells and peritoneal macrophages demonstrated the ability to release activin A.
  • This release was triggered by stimulation with agonists of Toll-like receptor (TLR) 2, 4, and 9.
  • These findings identify microglia and macrophages as key producers of activin A.

Conclusions:

  • Microglia and macrophages are significant sources of activin A during innate immune responses.
  • These immune cells contribute to the elevated activin A levels seen in bacterial meningitis and sepsis.
  • Activin A plays a role in the innate immune response, with microglia and macrophages being key mediators.

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