Pneumococcal meningitis and endotoxemia: A cross-sectional clinical study

Sylvie Nguyen1, Jeanne Godon2, Jean-Paul Pais de Barros3

  • 1Lipness Team, INSERM Research Centre LNC-UMR1231 and LabEx LipSTIC, University of Burgundy, Dijon, France.

Plos One
|May 21, 2025
PubMed
Abstract

Insights

Lipopolysaccharide (LPS) is not a key factor in pneumococcal meningitis inflammation. Studies show no significant difference in LPS levels between meningitis patients and healthy individuals, despite higher inflammatory markers in patients.

Area of Science:

  • Infectious Diseases
  • Immunology
  • Microbiology

Background:

  • Lipopolysaccharide (LPS) is a critical virulence factor in meningococcal and Haemophilus influenzae meningitis.
  • Pneumococcus, unlike other bacteria, does not produce LPS but may contribute to bacterial translocation during sepsis.
  • The role of LPS in pneumococcal meningitis-associated inflammation requires investigation.

Purpose of the Study:

  • To investigate the presence and role of lipopolysaccharide (LPS) in pneumococcal meningitis.
  • To determine if LPS contributes to the systemic inflammation observed in pneumococcal meningitis.

Main Methods:

  • Cross-sectional study of 24 pneumococcal meningitis patients and 34 healthy volunteers.
  • Measurement of plasma interleukin-6 and C-reactive protein as systemic inflammation markers.
  • Quantification of plasma LPS using liquid chromatography-tandem mass spectrometry (LC-MS/MS).

Main Results:

  • Pneumococcal meningitis patients exhibited significantly elevated C-reactive protein and interleukin-6 levels compared to healthy controls.
  • No significant difference was found in plasma lipopolysaccharide concentrations between meningitis patients and healthy volunteers.
  • These findings indicate that LPS is not a primary driver of inflammation in severe pneumococcal meningitis.

Conclusions:

  • Lipopolysaccharide (LPS) does not appear to be a significant determinant of excessive inflammation in severe pneumococcal meningitis.
  • The inflammatory response in pneumococcal meningitis is likely driven by factors other than LPS.
  • Further research is needed to elucidate the specific mechanisms of inflammation in pneumococcal meningitis.

Related Concept Videos

Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

The pathophysiology of pneumonia involves the following steps:
4.7K
Pneumonia III: Complications and Assessment01:30

Pneumonia III: Complications and Assessment

Pneumonia poses the potential for numerous complications that warrant consideration. These complications include the following:
1.4K
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
31
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
45
Pneumonia I: Introduction01:29

Pneumonia I: Introduction

Pneumonia is an infection of the lower respiratory tract that leads to inflammation of the lung parenchyma, often resulting in the accumulation of inflammatory exudate in the alveoli and airways. Unlike the watery, low-protein fluid exudate in pulmonary edema, the exudate in this case is a thick fluid rich in immune cells, proteins, and debris produced during infection and inflammation.This impairs gas exchange and can lead to consolidation of lung tissue. The infection may be caused by a...
58