Ravi Jain1, Sharon Waldvogel-Thurlow1, Richard Darveau2, Richard Douglas1. 1. Department of Surgery, The University of Auckland, Grafton, Auckland, New Zealand. 2. Department of Periodontics and Oral Health Sciences, University of Washington, Seattle, WA.
Abstract
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.
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.
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