Transient increase of microglial C1q expression in the circumventricular organs of adult mouse during LPS-induced inflammation

Cell Biochem Funct. 2020 Jun;38(4):392-400. doi: 10.1002/cbf.3477. Epub 2020 Jan 6.

Abstract

The circumventricular organs (CVOs) are the brain regions that lack the blood-brain barrier and allow free entry of blood-derived molecules, offering specialized niche to initiate rapid and early neuroinflammatory responses in the brain. Complement component 1q (C1q) is shown to be the first recognition component of the complement pathway and has a crucial function in the brain under pathological conditions. In the present study, we found that C1q expression in CX3CR1-positive microglia was increased in the CVOs and their neighbouring brain regions of adult mice at 1 day after a single administration of 1 mg/kg lipopolysaccharide (LPS), whereas it returned to control levels at 3 days after LPS stimulation. C1q expression was also seen to localize at synapsin-positive presynaptic axonal terminals in various brain regions. Thus, the present study demonstrates a transient upregulation of microglial C1q expression in the CVOs and their adjacent brain regions, indicating that a transient upregulation of C1q is possibly concerned with physiological responses at early phase of brain inflammation. SIGNIFICANCE OF THE STUDY: The circumventricular organs (CVOs) are specialized brain regions that lack the blood-brain barrier (BBB) and initiate neuroinflammatory responses in the brains. The present study showed that the expression of complement protein C1q was highly increased in microglia of the CVOs and their adjacent brain regions. Moreover, C1q expression was observed to localize specifically at presynaptic axonal terminals in the CVOs and their neighbouring brain regions. Thus, the present study indicates that C1q is possibly correlated with physiological responses at early phase of brain inflammation.

Keywords: brain; complement pathway; immunohistochemistry; inflammation; microglia.

MeSH terms

  • Animals
  • Axons / metabolism
  • Axons / pathology
  • Brain / metabolism*
  • Brain / pathology
  • Circumventricular Organs / metabolism*
  • Circumventricular Organs / pathology
  • Complement C1q / biosynthesis*
  • Gene Expression Regulation / drug effects*
  • Inflammation / chemically induced
  • Inflammation / metabolism
  • Inflammation / pathology
  • Lipopolysaccharides / toxicity*
  • Mice
  • Microglia / metabolism*
  • Microglia / pathology

Substances

  • Lipopolysaccharides
  • Complement C1q