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CXCL16 contributes to neutrophil recruitment to cerebrospinal fluid in pneumococcal meningitis

Bianca Woehrl1, Matthias Klein, Tobias A Rupprecht

  • 1Department of Neurology, Klinikum Grosshadern, Ludwig Maximilians University, Munich, Germany. Bianca.Woehrl@med.uni-muenchen.de

The Journal of Infectious Diseases
|September 30, 2010
PubMed

Insights

This study reveals CXCL16 is increased in pneumococcal meningitis, acting as a neutrophil chemoattractant in cerebrospinal fluid. Its regulation involves Toll-like receptor signaling, impacting disease progression.

Area of Science:

  • Immunology
  • Neuroscience
  • Infectious Diseases

Background:

  • Pneumococcal meningitis is a serious infection with significant morbidity.
  • Neutrophil recruitment to the central nervous system is critical in meningitis pathogenesis.
  • The role of specific chemokines, like CXCL16, in pneumococcal meningitis remains incompletely understood.

Purpose of the Study:

  • To investigate the expression and function of CXCL16 in the context of pneumococcal meningitis.
  • To elucidate the signaling pathways involved in CXCL16 regulation during infection.
  • To determine the impact of CXCL16 on neutrophil recruitment and cerebrospinal fluid pleocytosis.

Main Methods:

  • Analysis of CXCL16 expression in macrophages, neutrophils, and endothelial cells stimulated with Streptococcus pneumoniae.
  • Measurement of CXCL16 levels in cerebrospinal fluid from patients and in mouse models of pneumococcal meningitis.
  • Investigation of CXCL16 regulation via Toll-like receptor (TLR) 2/TLR4 and MyD88 signaling pathways.
  • In vivo neutralization of CXCL16 using antibodies in a mouse model of meningitis.
  • In vitro assessment of murine neutrophil migration towards CXCL16 using transwell assays.

Main Results:

  • CXCL16 expression was upregulated in macrophages upon pneumococcal stimulation, and in cerebrospinal fluid and brain tissue of infected patients and mice.
  • CXCL16 upregulation in vivo was dependent on Toll-like receptor 2/4 and MyD88 signaling.
  • Neutralization of CXCL16 reduced cerebrospinal fluid pleocytosis in infected mice.
  • Murine neutrophils expressed the CXCL16 receptor CXCR6 and migrated towards CXCL16 in vitro.

Conclusions:

  • CXCL16 is upregulated during pneumococcal meningitis and plays a role in neutrophil recruitment.
  • CXCL16 acts as a chemoattractant for neutrophils in the cerebrospinal fluid during early stages of the infection.
  • Targeting CXCL16 may represent a potential therapeutic strategy for managing pneumococcal meningitis.

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