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Table · dataset · 2026

Video 1_Sleep fragmentation frequency is associated with distinct immune, microbial, and barrier-related profiles in DSS-induced colitis in mice.mp4

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Background<p>Sleep fragmentation is common in inflammatory bowel disease, but whether different fragmentation frequencies are associated with distinct biological responses during colitis remains unclear.

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This study examined endpoint-specific responses to low- and high-frequency sleep fragmentation in DSS-induced colitis in mice.</p>Methods<p>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<sup>+</sup> T-cell subsets, fecal microbiota composition, and fecal SCFAs were assessed.</p>Results<p>Clinical and macroscopic indices varied across experimental groups, but corrected comparisons among DSS-treated groups were not significant.

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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.</p>Conclusions<p>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.</p>

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