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Characterization of Inflammatory Responses During Intranasal Colonization with Streptococcus pneumoniae
Published on: January 17, 2014
Blood‒Brain Barrier Pathology and CNS Outcomes in Streptococcus pneumoniae Meningitis
Belinda Yau1, Nicholas H Hunt2, Andrew J Mitchell3
1Molecular Immunopathology Unit, Bosch Institute and School of Medical Sciences, University of Sydney, Sydney 2006, Australia. belinda.yau@sydney.edu.au.
Abstract:
Streptococcus pneumoniae is a major meningitis-causing pathogen globally, bringing about significant morbidity and mortality, as well as long-term neurological sequelae in almost half of the survivors. Subsequent to nasopharyngeal colonisation and systemic invasion, translocation across the blood‒brain barrier (BBB) by S. pneumoniae is a crucial early step in the pathogenesis of meningitis. The BBB, which normally protects the central nervous system (CNS) from deleterious molecules within the circulation, becomes dysfunctional in S. pneumoniae invasion due to the effects of pneumococcal toxins and a heightened host inflammatory environment of cytokines, chemokines and reactive oxygen species intracranially. The bacteria‒host interplay within the CNS likely determines not only the degree of BBB pathological changes, but also host survival and the extent of neurological damage. This review explores the relationship between S. pneumoniae bacteria and the host inflammatory response, with an emphasis on the BBB and its roles in CNS protection, as well as both the acute and long-term pathogenesis of meningitis.
Insights
Streptococcus pneumoniae causes meningitis by breaching the blood-brain barrier (BBB). This review examines how bacterial invasion and host inflammation impact the BBB, leading to neurological damage.
Area of Science:
- Neuroscience
- Infectious Diseases
- Immunology
Background:
- Streptococcus pneumoniae is a leading global cause of meningitis, resulting in high mortality and long-term neurological deficits.
- Bacterial translocation across the blood-brain barrier (BBB) is a critical step in meningitis pathogenesis.
- Pneumococcal toxins and host inflammatory responses disrupt BBB integrity, compromising central nervous system (CNS) protection.
Purpose of the Study:
- To explore the intricate relationship between Streptococcus pneumoniae and host inflammatory responses.
- To emphasize the role of the blood-brain barrier (BBB) in CNS protection and meningitis pathogenesis.
- To review the acute and long-term neurological damage resulting from pneumococcal meningitis.
Main Methods:
- Literature review of studies on Streptococcus pneumoniae pathogenesis.
- Analysis of the mechanisms underlying BBB dysfunction during pneumococcal meningitis.
- Examination of host inflammatory mediators, including cytokines and chemokines.
Main Results:
- Streptococcus pneumoniae invades the CNS by disrupting the BBB.
- Host inflammatory responses, including cytokines and reactive oxygen species, exacerbate BBB damage.
- The interplay between bacteria and host inflammation dictates BBB integrity, survival, and neurological sequelae.
Conclusions:
- Understanding the bacteria-host-BBB interaction is crucial for developing effective meningitis treatments.
- The BBB's dysfunction is a key factor in the severity and long-term consequences of pneumococcal meningitis.
- Further research into neuroinflammation and BBB repair is needed to mitigate neurological damage.
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