Related Experiment Video
Updated: Mar 23, 2026

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
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.
Background:
The role of bacteria in the etiology of chronic rhinosinusitis (CRS) is not fully understood. Commensal bacteria may have a significant impact on the development of normal paranasal sinus anatomy and mucosal immunity, as they do in the gut. Studying the paranasal sinuses of germ-free (GF) mice may provide some insight into the effect of commensal bacteria on sinus structure and mucosal function.
Methods:
The paranasal sinuses of 5 GF mice were compared to 5 pathogen-free normal mice. Mice heads underwent computed tomography and images were compared for pneumatization and geometry of the sinuses. Histologically, slides were examined by light microscopy and compared for mucosal thickness, epithelial thickness, cilia, collagen, goblet cells, and nasal-associated lymphatic tissue (NALT).
Results:
No radiological differences were seen between groups. Overall, GF mice were found to have thinner mucosa (Δ 15.2 ± 5.2 μm, p = 0.004), thinner epithelium (Δ 5.5 ± 2.6 μm, p = 0.037), more collagen (Δ 5.8% ± 1.6%, p < 0.001), fewer goblet cells (Δ 29.3 ± 5.4, p < 0.001), and less NALT (Δ 14,900 ± 6700 μm(2) , p = 0.04). Subanalysis by region revealed significant differences for GF mice in the middle (thinner mucosa, thinner epithelium, fewer cilia, and more collagen) and posterior (fewer goblet cells) sinus sections.
Conclusion:
The results of this study demonstrate that commensal microbiota significantly contribute to the structure and function of murine paranasal sinuses. Therefore, changes in commensal microbiota associated with CRS may alter the normal microbe host dialogue in humans and be implicated in the pathogenesis of CRS.
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.
More Related Videos
07:43A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice
Published on: September 28, 2016
09:12Characterization of Inflammatory Responses During Intranasal Colonization with Streptococcus pneumoniae
Published on: January 17, 2014