641: Depth of 16S rRNA sequencing required for characterization of microbial composition in the vaginal, oral, and rectal compartments in pregnancy

Our previous study showed a reduction of anxiety-like behavior in offspring rats suffered from prenatal cold stress; whether this was related to changes in the offspring gut microbiota is unclear. To obtain the evidence for the role of the gut microbiota in prenatal cold stress offspring, 16S rRNA sequencing technology was used. Male and female offspring rat feces were collected from a room temperature group and a prenatal cold stress group (n ≥ 8) for microbial DNA extraction, followed by 16S rRNA sequencing. The results indicated that prenatal cold stress could change the offspring’s gut microbiota composition. Prenatal cold stress significantly upregulates Lactobacillus, Lactobacillus_gasseri, Bacteroides, and Bacteroides-acidifaciens in female offspring, whereas prenatal cold stress significantly reduced Lachnospiraceae and Prevotellaceae in male offspring. These data showed the characterization of gut microbiota in prenatal cold stress offspring rats, and these data suggest that microbiological intervention in the future can potentially prevent the negative effects caused by cold stress to animals.

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Comparative Analyses of Subgingival Microbiome in Chronic Periodontitis Patients with and Without IgA Nephropathy by High Throughput 16S rRNA Sequencing

Cellular Physiology and Biochemistry ◽

10.1159/000490029 ◽

2018 ◽

Vol 47 (2) ◽

pp. 774-783 ◽

Cited By ~ 7

Author(s):

Yali Cao ◽

Min Qiao ◽

Zhigang Tian ◽

Yan Yu ◽

Baohua Xu ◽

...

Keyword(s):

16S Rrna ◽

Chronic Periodontitis ◽

Alveolar Bone ◽

Gingival Recession ◽

Chronic Inflammatory Disease ◽

16S Rrna Sequencing ◽

Periodontal Pocket ◽

Microbial Composition ◽

Comparative Analyses ◽

Rrna Sequencing

Background/Aims: Periodontitis is a prevalent chronic inflammatory disease caused by enhanced inflammation induced by dysbiotic microbes forming on subgingival tooth sites, which may disturb the balance of the microbial composition in the biofilm and finally result in the progressive destruction of the periodontal ligament and alveolar bone with periodontal pocket formation and/or gingival recession. Methods: To elucidate the correlation between subgingival microbiome and IgAN incidence in CP (chronic periodontitis at severe levels) patients, subgingival plaque samples were collected from CP patients without IgAN (Control) and CP patients with IgAN (Disease). 16S rRNA sequencing and comparative analyses of plaque bacterial microbiome between Control and Disease were performed. Results: Subgingival microbial diversity in Disease was a little higher than that in Control. Besides, significant differences were found in subgingival microbiome between Disease and Control. Compared with that in Control, at phylum level, the abundances of Proteobacteria and Actinobacteria were significantly higher while the abundances of Bacteroidetes, Fusobacteria, Spirochaetae, Synergistetes, and Saccharibacteria were significantly lower in Disease; at class level, the abundances of Betaproteobacteria, Bacilli, Actinobacteria, Flavobacteriia, and Gammaproteobacteria were significantly higher while the abundances of Bacteroidia, Fusobacteriia, Negativicutes, Clostridia, and Spirochaetes were significantly lower in Disease; at genus level, the abundances of Bergeyella, Capnocytophaga, Actinomyces, Corynebacterium, Comamonas, Lautropia, and Streptococcus were significantly higher while the abundances of Treponema and Prevotella were significantly lower in Disease. Conclusions: Our data indicated a correlation between the changes in subgingival microbial structure and IgAN incidence in CP patients, which might be used to predict IgAN incidence in CP patients.

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