Journal of Microbiology

Jing Cao

2 Articles

Role of melatonin in murine “restraint stress”-induced dysfunction of colonic microbiota: Rutao Lin , Zixu Wang , Jing Cao , Ting Gao , Yulan Dong , Yaoxing Chen; J. Microbiol. 2021;59(5):500-512. Published online February 25, 2021; DOI: https://doi.org/10.1007/s12275-021-0305-7

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Intestinal diseases caused by physiological stress have become a severe public health threat worldwide. Disturbances in the gut microbiota-host relationship have been associated with irritable bowel disease (IBD), while melatonin (MT) has antiinflammatory and antioxidant effects. The objective of this study was to investigate the mechanisms by which MT-mediated protection mitigated stress-induced intestinal microbiota dysbiosis and inflammation. We successfully established a murine restraint stress model with and without MT supplementation. Mice subjected to restraint stress had significantly elevated corticosterone (CORT) levels, decreased MT levels in their plasma, elevated colonic ROS levels and increased bacterial abundance, including Bacteroides and Tyzzerella, in their colon tract, which led to elevated expression of Toll-like receptor (TLR) 2/4, p-P65 and p-IκB. In contrast, supplementation with 20 mg/kg MT reversed the elevation of the plasma CORT levels, downregulated the colon ROS levels and inhibited the changes in the intestinal microbiota induced by restraint stress. These effects, in turn, inhibited the activities of TLR2 and TLR4, p-P65 and p-IκB, and decreased the inflammatory reaction induced by restraint stress. Our results suggested that MT may mitigate “restraint stress”-induced colonic microbiota dysbiosis and intestinal inflammation by inhibiting the activation of the NF-κB pathway.

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Melatonin attenuates microbiota dysbiosis of jejunum in short-term sleep deprived mice: Ting Gao , Zixu Wang , Jing Cao , Yulan Dong , Yaoxing Chen; J. Microbiol. 2020;58(7):588-597. Published online May 18, 2020; DOI: https://doi.org/10.1007/s12275-020-0094-4

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Abstract PDF

Our study demonstrated that sleep deprivation resulted in homeostasis disorder of colon. Our study goes deeper into the positive effects of melatonin on small intestinal microbiota disorder caused by sleep deprivation. We successfully established a multiplatform 72 h sleep deprivation mouse model with or without melatonin supplementation, and analyzed the change of small intestinal microbiota using high-throughput sequencing of the 16S rRNA. We found melatonin supplementation suppressed the decrease of plasma melatonin level in sleep deprivation mice. Meanwhile, melatonin supplementation improved significantly the reduction in OTU numbers and the diversity and richness of jejunal microbiota and the abundance of Bacteroidaeae and Prevotellaceae, as well as an increase in the Firmicutes-to-Bacteroidetes ratio and the content of Moraxellaceae and Aeromonadaceae in the jejunum of sleep deprived-mice. Moreover, melatonin supplementation reversed the change of metabolic pathway in sleep deprived-mice, including metabolism, signal transduction mechanisms and transcription etc, which were related to intestinal health. Furthermore, melatonin supplementation inverted the sleep deprivation-induced a decline of anti-inflammatory cytokines (IL-22) and an increase of the ROS and proinflammatory cytokines (IL-17) in jejunum. These findings suggested that melatonin, similar to a probiotics agent, can reverse sleep deprivation-induced small intestinal microbiota disorder by suppressing oxidative stress and inflammation response.

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