<p>Bloodstream infections (BSIs), caused by a diverse array of microbial pathogens, have emerged as key drivers of systemic inflammation that can compromise the integrity of blood-brain barrier (BBB) and trigger neuroinflammatory responses. This review highlights the pivotal role of BSIs in initiating neuroinflammation and accelerating the progression of neurodegenerative diseases (NDDs). Literature review shows that pathogens involved in BSIs can disrupt the BBB, activate neuroglial cells, and release pro-inflammatory cytokines, ultimately causing neuronal injury and fueling chronic neuroinflammation. Clinically, survivors of BSIs, especially those who experience sepsis, face a heightened risk of long-term neurological decline. While antimicrobial treatments remain essential, advanced therapeutic options such as psychedelics, immunomodulators, and nano pharmacology, gene therapies offer promising strategies to mitigate neuroinflammation and protect brain function. The review emphasizes the urgency of early intervention, particularly in sepsis patients, to prevent the onset of chronic NDDs and preserve cognitive health. A deeper understanding of the mechanisms underlying BSI-induced neuroinflammation will be critical in developing personalized treatments to reduce the neurological burden associated with these infections. Ultimately, this review aims to provide clinicians with insights into neuroprotective strategies that have shown promise in animal models of BSIs, with the potential to improve patient outcomes if validated in humans; further clinical studies are essential to translate these findings into effective therapies for long-term neurological consequences.</p>

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Bloodstream Infection-induced Neuroinflammation: from Systemic Infection To Brain Invasion

  • Gargee Anand,
  • Rijhul Lahariya

摘要

Bloodstream infections (BSIs), caused by a diverse array of microbial pathogens, have emerged as key drivers of systemic inflammation that can compromise the integrity of blood-brain barrier (BBB) and trigger neuroinflammatory responses. This review highlights the pivotal role of BSIs in initiating neuroinflammation and accelerating the progression of neurodegenerative diseases (NDDs). Literature review shows that pathogens involved in BSIs can disrupt the BBB, activate neuroglial cells, and release pro-inflammatory cytokines, ultimately causing neuronal injury and fueling chronic neuroinflammation. Clinically, survivors of BSIs, especially those who experience sepsis, face a heightened risk of long-term neurological decline. While antimicrobial treatments remain essential, advanced therapeutic options such as psychedelics, immunomodulators, and nano pharmacology, gene therapies offer promising strategies to mitigate neuroinflammation and protect brain function. The review emphasizes the urgency of early intervention, particularly in sepsis patients, to prevent the onset of chronic NDDs and preserve cognitive health. A deeper understanding of the mechanisms underlying BSI-induced neuroinflammation will be critical in developing personalized treatments to reduce the neurological burden associated with these infections. Ultimately, this review aims to provide clinicians with insights into neuroprotective strategies that have shown promise in animal models of BSIs, with the potential to improve patient outcomes if validated in humans; further clinical studies are essential to translate these findings into effective therapies for long-term neurological consequences.