Increasing evidence has emerged a tight link among the gut microbiota, host age and health status. This osculating interplay impedes the definition of gut microbiome features associated with host health from that in developmental stages. Consequently, gut microbiota-based prediction of health status is promising yet not well established. Here we firstly tracked shrimp gut microbiota (N = 118) over an entire cycle of culture; shrimp either stayed healthy or progressively transitioned into severe disease. The results showed that the gut microbiota were significantly distinct over shrimp developmental stages and disease progression. Null model and phylogenetic-based mean nearest taxon distance (MNTD) analyses indicated that deterministic processes that governed gut community became less important as the shrimp aged and disease progressed. The predicted gut microbiota age (using the profiles of age-discriminatory bacterial species as independent variables) fitted well (r = 0.996; P < 0.001) with the age of healthy subjects, while this defined trend was disrupted by disease. Microbiota-for-age Z-scores (MAZ, here defined as immaturity) were relative stable among healthy shrimp, but sharply decreased when disease emerged. By distinguishing between age- and disease- discriminatory taxa, we developed a model, bacterial indicators of shrimp health status, to diagnose disease from healthy subjects with 91.5% accuracy. Notably, the relative abundances of the bacterial indicators were indicative for shrimp disease severity. These findings, in aggregate, add our understanding on the gut community assembly patterns over shrimp developmental stages and disease progression. In addition, shrimp disease initiation and severity can be accurately diagnosed using gut microbiota immaturity and bacterial indicators.

IntroductionPeriodontitis is initiated and sustained by bacteria. However, the mechanism of bacteria induced periodontitis is still unknown. We hypothesized that bacterial components can affect the functions of stem cells in the periodontium. In this study, we comparatively investigated the influence of Lipopolysaccharide (LPS) on the osteogenesis potential of human periodontal ligament stem cells (PDLSCs) and bone marrow mesenchymal stem cells (BMMSCs).MethodsHuman PDLSCs and BMMSCs were harvested and mineralized nodule formation was assessed by alizarin red S staining. Expression level of osteogenic related gene was detected by quantitative RT-PCR (qRT-PCR). The expression of Toll-like receptor 4 (TLR4) and its downstream signaling pathway were examined by western blot. The role of TLR4 and related signaling pathway in LPS impairing the osteogenic potential of human PDLSCs and BMMSCs were also studied by alizarin red S staining and qRT-PCR. Experimental periodontitis was induced in adult Sprague–Dawley rats and the alveolar bone loss was measured by micro computed tomography analysis. The expression of alkaline phosphatase (ALP) was assessed by immunohistochemistry and the number of osteoclasts was shown by Tartrate-resistant acid phosphatase (TRAP) staining.ResultsLPS decreased the osteogenic differentiation of human PDLSCs through TLR4 regulated nuclear factor (NF)-κB pathway, but not for BMMSCs. Blocking TLR4 or NF-κB signaling partially reversed the decreased osteogenic potential of PDLSCs and prevented the alveolar bone loss caused by LPS experimental periodontitis in rats. The ALP expression in the periodontal ligament was elevated after treatment with anti-TLR4 antibody or pyrrolidinedithiocarbamate, whereas there was no statistical significance among groups for the number of osteoclasts.ConclusionsThese data suggest that LPS can activate TLR4 regulated NF-κB pathway of human PDLSCs, thus decreasing their osteogenic potential. Blockage of TLR4 or NF-κB pathway might provide a new approach for periodontitis treatment.

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