Differences in the paranasal sinuses between germ-free and pathogen-free mice

Ravi Jain1, Sharon Waldvogel-Thurlow1, Richard Darveau2

  • 1Department of Surgery, The University of Auckland, Grafton, Auckland, New Zealand.

Abstract

Insights

Germ-free mice exhibit altered paranasal sinus structure, including thinner mucosa and epithelium, indicating commensal bacteria are crucial for normal sinus development and function. This finding suggests microbial changes may play a role in chronic rhinosinusitis (CRS).

Area of Science:

  • Microbiology
  • Immunology
  • Otolaryngology

Background:

  • The role of bacteria in chronic rhinosinusitis (CRS) pathogenesis is not fully understood.
  • Commensal bacteria, similar to their role in the gut, may influence paranasal sinus anatomy and mucosal immunity.
  • Germ-free (GF) mouse models offer a unique approach to study the impact of commensal bacteria on sinus development.

Purpose of the Study:

  • To investigate the structural and functional effects of commensal microbiota on murine paranasal sinuses.
  • To compare the sinus anatomy and mucosal characteristics of germ-free mice with pathogen-free controls.

Main Methods:

  • Computed tomography (CT) was used to assess sinus pneumatization and geometry in GF and control mice.
  • Histological analysis examined mucosal thickness, epithelial thickness, cilia, collagen, goblet cells, and nasal-associated lymphatic tissue (NALT).

Main Results:

  • No significant radiological differences were observed between GF and control mice.
  • GF mice displayed significantly thinner mucosa and epithelium, increased collagen deposition, fewer goblet cells, and reduced NALT.
  • Regional analysis revealed differences in middle and posterior sinus sections, including thinner mucosa, thinner epithelium, fewer cilia, and more collagen in GF mice.

Conclusions:

  • Commensal microbiota are essential for the normal development and structure of murine paranasal sinuses.
  • Alterations in commensal microbiota composition could disrupt the host-microbe dialogue, potentially contributing to CRS pathogenesis.

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