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Experimental Human Pneumococcal Carriage
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Experimental Human Pneumococcal Carriage

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Increased hypothalamic microglial activation after viral-induced pneumococcal lung infection is associated with

Hao Wang1, Melissa Blackall1, Luba Sominsky1

  • 1School of Health and Biomedical Sciences, RMIT University, PO Box 71, Bundoora, VIC, 3083, Australia.

Journal of Neuroinflammation
|July 8, 2018
PubMed
Abstract

Insights

Lung co-infection with bacteria and viruses activates microglia in the hypothalamus, increasing neuroinflammation. Serum amyloid A (SAA) drives this response, which can be blocked by the anti-inflammatory AT-RvD1.

Area of Science:

  • Neuroscience
  • Immunology
  • Infectious Diseases

Background:

  • Respiratory infections with both bacteria and viruses cause more severe lung pathology and inflammation.
  • The neuroinflammatory effects of such co-infections are not well understood.

Purpose of the Study:

  • To investigate the neuroinflammatory consequences of co-infection with Streptococcus pneumoniae (S. pneumoniae) and influenza A virus (IAV) in a mouse model.
  • To examine the role of microglia and serum amyloid A (SAA) in the brain during co-infection.

Main Methods:

  • Utilized a mouse co-infection model of S. pneumoniae and IAV lung infection.
  • Isolated microglia for ex vivo stimulation with pneumococcus or SAA.
  • Measured cytokine expression and microglial morphology in the hypothalamus.

Main Results:

  • Co-infection significantly increased amoeboid microglia and pro-inflammatory cytokines (TNFα, IL-1β, IL-6, CCL-2) in the hypothalamus.
  • Pneumococcus was detected in the hypothalamus of co-infected mice.
  • SAA levels were markedly increased in co-infected mice, and SAA stimulated microglia to produce inflammatory cytokines, an effect blocked by AT-RvD1.

Conclusions:

  • Lung co-infection activates microglia and increases inflammatory cytokine expression in the hypothalamus.
  • SAA is a potent stimulus for microglia during co-infection, more so than pneumococci.
  • Targeting the Fpr2 receptor with pro-resolving agents like AT-RvD1 may help restore microglial homeostasis during severe respiratory infections.
Keywords:
MicrogliaNeuroinflammationPneumoniaResolvin-D1Serum amyloid A

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