Experimental findings show that Toxoplasma gondii infection reduces fractalkine in neurons, suggesting implications for neuroinflammation and blood-brain barrier integrity.
Key Points
In Toxoplasma gondii-infected neurons, fractalkine shedding is impaired, leading to microglial activation.
Nine angiogenic-regulating factors were identified in neuronal conditioned media, indicating diverse signaling effects.
In vivo, CX3CL1 receptor expression increased while levels of its soluble form decreased post-infection.
Targeting fractalkine may provide a new approach to mitigate neurocognitive damage associated with toxoplasmosis.