Estrogen inhibits the overgrowth of Escherichia coli in the rat intestine under simulated microgravity
نویسندگان
چکیده
Microgravity can affect many aspects of intestinal homeostasis, leading to an increased risk of colitis. Estrogen, the most frequently affected hormone when under simulated microgravity, regulates the permeability of the colonic mucosa barrier. The associations between alterations in intestinal microbiota and increased susceptibility under microgravity have not been thoroughly elucidated. The aim of the present study was to evaluate the changes in intestinal microbiota under simulated microgravity and to investigate the protective effect of estrogen against those changes. The hindlimb unweighting (HU) model was used to simulate microgravity in rats. Estrogen was administered via intramuscular injection. Amplicons of the V3 variable regions of bacterial 16S rDNA were analyzed using denaturing gradient gel electrophoresis (DGGE), cloning and sequencing. Several specific bacterial groups were assayed using quantitative‑polymerase chain reaction. Bacterial translocation was evaluated by detecting serum lipopolysaccharide (LPS) and LPS binding protein (LBP) levels. DGGE profiles generated by universal primers revealed minor, though specific, changes in bacterial communities under simulated microgravity, particularly the band matching the sequence of Escherichia coli (E. coli). The quantification of 16S RNA revealed increased numbers of Bacteroides fragilis, E. coli and Fusobacterium nucleatum; however, Bifidobacteria longum significantly decreased under microgravity. Estrogen inhibited the overgrowth of E. coli, and decreased the levels of LBS and LBP under simulated microgravity. These results demonstrated that simulated microgravity alters the intestinal microflora and may contribute to bacterial translocation in the gut mucosa. The data also suggested that further investigations evaluating the administration of estrogen to protect against microgravity‑associated diseases may be required.
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عنوان ژورنال:
دوره 17 شماره
صفحات -
تاریخ انتشار 2018