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Differences in the paranasal sinuses between germ‐free and pathogen‐free mice
Author(s) -
Jain Ravi,
WaldvogelThurlow Sharon,
Darveau Richard,
Douglas Richard
Publication year - 2016
Publication title -
international forum of allergy and rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.503
H-Index - 46
eISSN - 2042-6984
pISSN - 2042-6976
DOI - 10.1002/alr.21712
Subject(s) - paranasal sinuses , medicine , sinus (botany) , pathology , sinusitis , epithelium , anatomy , cilium , biology , immunology , microbiology and biotechnology , botany , genus
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.