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Published on: May 2, 2018
Crosstalk between imbalanced gut microbiota caused by antibiotic exposure and rotavirus replication in the intestine
1School of Biology, Food and Environment, Hefei University, Hefei 230032, Anhui, China.
Insights
Asymptomatic adults can spread rotavirus (RV). Antibiotic exposure disrupts gut bacteria, increasing RV replication risk and potential health issues. Further research is needed.
Area of Science:
- Virology
- Microbiology
- Gastroenterology
Background:
- Rotavirus (RV) is a major cause of infantile diarrhea, primarily transmitted via the fecal-oral route.
- Asymptomatic adult carriers are increasingly recognized as a significant source of RV transmission.
- Understanding RV replication mechanisms in adult intestines is crucial for public health.
Purpose of the Study:
- To investigate the link between animal-derived food intake and antibiotic levels in adults.
- To compare gut microbiota structures in RV carriers versus healthy individuals.
- To determine the impact of lipopolysaccharide (LPS) on RV replication.
Main Methods:
- Recruitment of healthy volunteers and asymptomatic RV carriers.
- Analysis of urine antibiotic levels and gut microbiota composition.
- In vivo and in vitro experiments assessing LPS effects on RV replication.
Main Results:
- 10% of participants were asymptomatic RV carriers.
- High animal-derived food intake correlated with elevated urine antibiotic levels.
- RV carriers exhibited disrupted gut microbiota with antibiotic-resistant gram-negative bacteria and high LPS levels.
- Penicillin-induced gut dysbiosis and LPS exposure promoted RV replication.
Conclusions:
- Imbalanced gut microbiota due to antibiotic exposure is a key factor in RV replication.
- This dysbiosis increases the risk of RV-related health complications.
- Findings highlight the importance of gut health in preventing viral infections.
Objective:
Rotavirus (RV), one of non-enveloped double-strained RNA viruses, can cause infantile diarrheal illness. It is widely accepted that RV is transmitted mainly via feces-oral route. However, infected asymptomatic adults are becoming the source of infection. It is necessary to explore the underlying mechanism of RV replication in adult's intestine.
Methods:
After recruiting healthy volunteers and RV asymptomatic carriers, we firstly investigated the association of animal-derived food intake with antibiotic level in urine samples. Secondly, we compared the difference in the structure of gut microbiota, and identified the taxa that most likely explained the difference. Finally, we investigated the impact of lipopolysaccharide (LPS), produced by gram-negative bacteria, on RV replication in vivo and in vitro.
Results:
We found that 10% of participants were RV asymptomatic carriers in our study. High intake of animal-derived food was positively correlated to antibiotic level in urine samples. The disrupted gut microbiota in RV carriers was characterized by high abundance of antibiotic resistant gram-negative bacteria and high level of LPS. The disrupted gut microbiota caused by penicillin treatment was benefit to RV replication in vivo. LPS enhanced RV thermal stability in vitro.
Conclusions:
Our findings suggest that the imbalanced gut microbiota caused by antibiotic exposure plays an important role in RV replication, and brings risk to health complications.
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