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Oxytocin ameliorates KCC2 decrease induced by oral bacteria-derived LPS that affect rat primary cultured cells and

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Oral bacteria lipopolysaccharides (LPSs) impair central nervous system (CNS) function by reducing KCC2 transporter expression, altering GABAergic signaling. Oxytocin may counteract these effects, offering potential for treating LPS-induced brain disorders.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Neuroinflammation, often stress-induced, impairs central nervous system (CNS) function.
  • Lipopolysaccharides (LPSs) are potent inducers of neuroinflammation.
  • KCC2 transporter dysfunction is implicated in CNS disorders and behavioral problems.

Purpose of the Study:

  • To investigate the impact of LPSs from oral bacteria on CNS function, specifically KCC2 expression and GABAergic signaling.
  • To elucidate the molecular mechanisms underlying LPS-induced KCC2 inactivation.
  • To explore potential therapeutic interventions for LPS-induced brain dysfunction.

Main Methods:

  • Cultured PC-12 cells and primary rat cells were treated with LPSs from oral bacteria (P. gingivalis) and E. coli.
  • Gene expression analysis (TLR4, IL-1β, REST) and KCC2 transporter levels were assessed.
  • GABA function was evaluated, and the involvement of GSK3β signaling was investigated.
  • The effects of oxytocin and vasopressin on LPS-induced changes were examined.

Main Results:

  • LPS from P. gingivalis, but not E. coli, reduced KCC2 expression in neuronal cells.
  • LPS treatment activated TLR4, IL-1β, and REST, leading to KCC2 inactivation.
  • GABAergic function shifted from inhibitory to excitatory following P. gingivalis LPS exposure.
  • Oxytocin, by inhibiting GSK3β, rescued LPS-induced KCC2 reduction, while vasopressin did not.

Conclusions:

  • LPSs from oral bacteria, unlike those from E. coli, elevate the risk for brain disorders.
  • Oxytocin shows promise as a therapeutic agent for psychiatric and other brain disorders linked to oral bacterial LPS exposure.
  • Targeting GSK3β signaling offers a potential strategy for mitigating neuroinflammation-induced CNS dysfunction.