Laryngoscope investigative otolaryngology · 2025
Induced Chronic Rhinosinusitis in Rats Leads to Secondary Changes in Sinonasal Microbiota.
СтатьяНазвание и аннотация: Перевод в очереди
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Barriga-Chambi Fernanda, Ccami-Bernal Fabricio, Zela-Coila Frank, Hernandez-Caycho Marial, Mares-Cuadros Claudia, Salas-Palma Marcos, Ballón-Echegaray Jorge, Torres Renato
Аннотация
BACKGROUND: The microbiota may play a role in maintaining and perpetuating inflammation in chronic rhinosinusitis (CRS). This study aimed to induce CRS in rats and evaluate microbiota composition compared to controls.
METHODS: Sixteen male Wistar rats were used. Eight rats received intranasal instillations of Aspergillus oryzae protease and ovalbumin three times weekly for 12 weeks (CRS group). The remaining eight received PBS (control group) under the same conditions. At week 13, microbiological samples were surgically collected, and the rats were euthanized. Microbiological cultures for aerobic, anaerobic bacteria and fungi were performed, and colonies were identified using MALDI-TOF MS. Relative abundance was analyzed at the phylum and genus levels, and species richness was assessed using the Chao1 index. Histopathological analysis evaluated mucosal, vascular, and epithelial changes to confirm chronic inflammation.
RESULTS: Histopathological changes were more frequent in the CRS group compared to controls, especially mucosal changes (100% vs. 25%; p = 0.01, Chi-square test). Firmicutes were more abundant in CRS rats (60.3% vs. 38.4%), driven by an increase in Staphylococcus (33.6% vs. 77.7%). Species richness was higher in the CRS group (Chao1: 85.0 ± 23.3 [61.7-108.3]) compared to controls (31.3 ± 9.0 [22.2-40.3]; p = 0.004; Mann-Whitney U test).
CONCLUSIONS: Chronic inflammation induces significant microbiota changes, with an increase of species richness in the CRS group. These findings suggest microbiota shifts may result from inflammatory environments rather than being the primary cause.
LEVEL OF EVIDENCE: Basic science.
METHODS: Sixteen male Wistar rats were used. Eight rats received intranasal instillations of Aspergillus oryzae protease and ovalbumin three times weekly for 12 weeks (CRS group). The remaining eight received PBS (control group) under the same conditions. At week 13, microbiological samples were surgically collected, and the rats were euthanized. Microbiological cultures for aerobic, anaerobic bacteria and fungi were performed, and colonies were identified using MALDI-TOF MS. Relative abundance was analyzed at the phylum and genus levels, and species richness was assessed using the Chao1 index. Histopathological analysis evaluated mucosal, vascular, and epithelial changes to confirm chronic inflammation.
RESULTS: Histopathological changes were more frequent in the CRS group compared to controls, especially mucosal changes (100% vs. 25%; p = 0.01, Chi-square test). Firmicutes were more abundant in CRS rats (60.3% vs. 38.4%), driven by an increase in Staphylococcus (33.6% vs. 77.7%). Species richness was higher in the CRS group (Chao1: 85.0 ± 23.3 [61.7-108.3]) compared to controls (31.3 ± 9.0 [22.2-40.3]; p = 0.004; Mann-Whitney U test).
CONCLUSIONS: Chronic inflammation induces significant microbiota changes, with an increase of species richness in the CRS group. These findings suggest microbiota shifts may result from inflammatory environments rather than being the primary cause.
LEVEL OF EVIDENCE: Basic science.