Frontiers in immunology · 2026
Sleep fragmentation frequency is associated with distinct immune, microbial, and barrier-related profiles in DSS-induced colitis in mice.
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Tu Ming-Shih, Fan Ting-An, Huang Yueh-Hsiang, Wu Ren-Chin, Kuo Chia-Jung, Chen Ning-Hung, Chuang Li-Pang, Lin Shih-Wei, Chen Yen-Lung, Yang Huang-Yu, Liu Geng-Hao
Аннотация
BACKGROUND: Sleep fragmentation is common in inflammatory bowel disease, but whether different fragmentation frequencies are associated with distinct biological responses during colitis remains unclear. This study examined endpoint-specific responses to low- and high-frequency sleep fragmentation in DSS-induced colitis in mice.
METHODS: Male C57BL/6 mice were assigned to Control, DSS, DSS with low-frequency sleep fragmentation (DSS+LSF), DSS with high-frequency sleep fragmentation (DSS+HSF), or high-frequency sleep fragmentation alone (HSF). Colitis was induced with 2% DSS for 7 days. Sleep fragmentation was applied for 12 h/day during the light phase at 60 sweeps/h for LSF or 240 sweeps/h for HSF. Clinical indices, histology, epithelial barrier-associated proteins, inflammatory and stress-related markers, colonic CD4+ T-cell subsets, fecal microbiota composition, and fecal SCFAs were assessed.
RESULTS: Clinical and macroscopic indices varied across experimental groups, but corrected comparisons among DSS-treated groups were not significant. Plasma corticosterone was increased in both DSS+LSF and DSS+HSF, whereas MPO was higher in DSS+LSF than in DSS+HSF. Colonic Th2 proportions were higher in DSS+HSF than in DSS and DSS+LSF. Other histological, barrier-associated, inflammatory, and metabolic findings were primarily descriptive.
CONCLUSIONS: Low- and high-frequency sleep fragmentation were associated with distinct, endpoint-specific response profiles during DSS-induced colitis rather than a simple linear increase in disease severity. These findings support frequency-associated, domain-specific responses and warrant further longitudinal and mechanistic investigation.
METHODS: Male C57BL/6 mice were assigned to Control, DSS, DSS with low-frequency sleep fragmentation (DSS+LSF), DSS with high-frequency sleep fragmentation (DSS+HSF), or high-frequency sleep fragmentation alone (HSF). Colitis was induced with 2% DSS for 7 days. Sleep fragmentation was applied for 12 h/day during the light phase at 60 sweeps/h for LSF or 240 sweeps/h for HSF. Clinical indices, histology, epithelial barrier-associated proteins, inflammatory and stress-related markers, colonic CD4+ T-cell subsets, fecal microbiota composition, and fecal SCFAs were assessed.
RESULTS: Clinical and macroscopic indices varied across experimental groups, but corrected comparisons among DSS-treated groups were not significant. Plasma corticosterone was increased in both DSS+LSF and DSS+HSF, whereas MPO was higher in DSS+LSF than in DSS+HSF. Colonic Th2 proportions were higher in DSS+HSF than in DSS and DSS+LSF. Other histological, barrier-associated, inflammatory, and metabolic findings were primarily descriptive.
CONCLUSIONS: Low- and high-frequency sleep fragmentation were associated with distinct, endpoint-specific response profiles during DSS-induced colitis rather than a simple linear increase in disease severity. These findings support frequency-associated, domain-specific responses and warrant further longitudinal and mechanistic investigation.