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

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.