A role for fibroblast growth factor receptor 1 in the pathogenesis of Neisseria meningitidis

Area of Science:

• Microbiology
• Cell Biology
• Pathogenesis

Background:

• Neisseria meningitidis causes meningitis and sepsis.
• Bacterial adaptation involves cell surface receptor interactions, leading to signaling and cytoskeletal changes.
• Endothelial cell receptors are critical for pathogen entry into host tissues.

Purpose of the Study:

• To investigate the interaction between Neisseria meningitidis and Fibroblast Growth Factor Receptor 1-IIIc (FGFR1-IIIc).
• To determine the role of FGFR1-IIIc in meningococcal adhesion and invasion of endothelial cells.
• To compare the interaction capabilities among pathogenic and commensal Neisseria species.

Main Methods:

• Utilized human blood microvascular endothelial cells (HBMECs).
• Assessed meningococcal recruitment of FGFR1-IIIc to the cell surface.
• Evaluated the necessity of FGFR1-IIIc expression for HBMEC invasion.
• Compared interaction with pathogenic Neisseria gonorrhoeae and non-pathogenic Neisseria species.

Main Results:

• Neisseria meningitidis successfully recruits FGFR1-IIIc onto HBMECs.
• FGFR1-IIIc expression is essential for efficient meningococcal invasion of HBMECs.
• The capacity to interact with FGFR1-IIIc is conserved in Neisseria gonorrhoeae but absent in commensal Neisseria species.

Conclusions:

• FGFR1-IIIc is a significant host cell receptor exploited by Neisseria meningitidis.
• FGFR1-IIIc mediates meningococcal invasion of the microvasculature, including the blood-brain barrier.
• This interaction mechanism is specific to pathogenic Neisseria species, offering potential therapeutic targets.