The relationship between gut microbiota and inflammatory response, learning and memory in mice by sleep deprivation.

Objective: Sleep deprivation has developed into a common phenomenon, which can lead to inflammatory responses and cognitive impairment, but the underlying mechanism is ambiguous. Emerging evidence shows that gut microbiota plays a crucial role in theoccurrence and development of inflammatory and psychiatric diseases, possibly through neuroinflammation and the brain-gut axis. The current study investigated the influence of sleep deprivation on gut microbiota composition, pro-inflammatory cytokines, learning and memory in mice. Further, it explored whether changes in gut microbiota increase pro-inflammatory cytokine and induce learning and memory impairment. Methods: Healthy 8-week-old male C57BL/6J mice were randomly divided into the regular control group (RC), environmental control group (EC), and sleep deprivation group (SD). The sleep deprivation model was established by the Modified Multiple Platform Method. The experimental mice were subjected to sleep deprivation for 6h/d (8:00 am∼14:00 pm) in a sleep deprivation chamber, and the duration of sleep deprivation was 8 weeks. Morris water maze test to assess learning and memory in mice. Enzyme-Linked Immunosorbent Assay determined the concentrations of inflammatory cytokines. The changes in gut microbiota in mice were analyzed by 16S rRNA sequencing. Results: We found that SD mice had elevated latency of exploration to reach the hidden platform (p>0.05) and significantly decreased traversing times, swimming distance, and swimming time in the target zone when the hidden platform was removed (p<0.05). Sleep deprivation caused dysregulated expression in serum IL-1ß, IL-6, and TNF-α in mice, and the difference was significant (all p<0.001). Tannerellaceae, Rhodospirillales, Alistipes, and Parabacteroides were significantly increased in SD mice. Correlation analysis showed IL-1ß was positively correlated with the abundance of Muribaculaceae (r=0.497, p<0.05) and negatively correlated with the abundance of Lachnospiraceae (r=-0.583, p<0.05). The TNF-α was positively correlated with the abundances of Erysipelotrichaceae, Burkholderiaceae, and Tannerellaceae (r=0.492, r=0.646, r=0.726, all p<0.05). Conclusion: Sleep deprivation can increase pro-inflammatory cytokine responses and learning and memory impairment in mice and may be caused by the disorder of the microbiota. These findings of this study may open avenues for potential interventions that can relieve the detrimental consequences of sleep loss.

Iron supplementation and deworming during pregnancy reduces the risk of anemia and stunting in infants less than 2 years of age: a study from Sub-Saharan Africa.

BACKGROUND: In sub-Saharan Africa, infant anemia, stunting and low birth weight remains major public health problems. It is unclear whether prenatal iron supplementation and/or deworming can reduce the risk of infant stunting, anemia and low birth weight. The aim of this study was to investigate the relationship between iron supplementation and/or deworming and stunting, anemia, and low birth weight in infants under two years of age in sub-Saharan Africa. METHODS: Our studies examined pooled data from Demographic and Health Surveys (DHS) in twenty-three African countries collected between 2014 and 2020. childhood anemia and stunting in infants under the age of two were the primary outcomes. Iron supplementation and deworming during prenatal visits were the main exposure variables. A multivariate logistic regression model was used to investigate these relationships. RESULTS: The prevalence of stunting was 29.9%, severe stunting was 10.6%, childhood anemia was 74.3%, childhood severe anemia was 3.2%, and low birth weight was 16.4%, respectively. The use of prenatal iron supplementation alone was associated with a significant reduction of childhood anemia [aOR (95% CI) = 0.9 (0.8-1.0)]. Prenatal deworming alone was associated with a significantly reduced risk of stunting [aOR (95% CI) = 0.7 (0.8-1.0)], childhood anemia [aOR (95% CI) = 0.7 (0.8-0.9)], and low birth weight [aOR (95% CI) = 0.7 (0.8-1.0)]. Prenatal iron supplementation plus deworming or iron supplementation (with or without deworming) were not associated with childhood anemia, infant stunting and low birth weight. CONCLUSIONS: In Sub-Saharan Africa, prenatal deworming alone has the potential to improve infants' outcomes. Childhood anemia was improved with prenatal iron supplementation alone. Our recent findings indicate the necessity for prospective studies on the association between prenatal iron supplementation plus deworming and childhood anemia, stunting and low birth weight.