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Meningococcal resistance to antimicrobial peptides is mediated by bacterial adhesion and host cell RhoA and Cdc42

Miriam Geörg1, Lisa Maudsdotter, Raquel Tavares

  • 1Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.

Cellular Microbiology
|July 10, 2013
PubMed

Insights

Pathogenic bacteria like Neisseria meningitidis can resist antimicrobial peptides (AMPs) by adhering to host cells. This adhesion involves host cell signaling and cholesterol, protecting bacteria from AMP-mediated killing.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Antimicrobial peptides (AMPs) are crucial for innate immunity against pathogens.
  • Pathogenic bacteria have developed resistance mechanisms against AMPs.
  • The role of host epithelia in bacterial AMP resistance is not well understood.

Purpose of the Study:

  • To investigate how host pharyngeal epithelial cells influence Neisseria meningitidis resistance to AMPs.
  • To elucidate the mechanisms underlying adhesion-induced AMP resistance in N. meningitidis.

Main Methods:

  • Assessing N. meningitidis survival against AMPs (LL-37, MAP, alamethicin, polymyxin B) after adhesion to pharyngeal epithelial cells.
  • Investigating the role of RhoA and Cdc42 signaling pathways.
  • Analyzing the involvement of the actin cytoskeleton.
  • Examining the formation of cholesterol-rich membrane microdomains and the necessity of host cell cholesterol.

Main Results:

  • Adhesion to pharyngeal and airway epithelial cells conferred resistance to LL-37, MAP, and alamethicin, but not polymyxin B.
  • Inhibition of RhoA and Cdc42 signaling abolished adhesion-induced LL-37 resistance, independent of the actin cytoskeleton.
  • N. meningitidis induced cholesterol-rich membrane microdomains in host cells, and host cell cholesterol was essential for this resistance.

Conclusions:

  • N. meningitidis utilizes host epithelial cell signaling pathways (Rho GTPase-dependent) to enhance its resistance to certain AMPs.
  • The epithelial microenvironment, particularly cholesterol-rich membrane microdomains, is exploited by N. meningitidis for protection against LL-37.
  • Understanding these mechanisms could reveal new therapeutic strategies against bacterial infections.

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