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Background Microbiome big data from population-scale cohorts holds the key to unleash the power of microbiomes to overcome critical challenges in disease control, treatment and precision medicine. However, variations introduced during data generation and processing limit the comparisons among independent studies in respect of interpretability. Although multiple databases have been constructed as platforms for data reuse, they are of limited value since only raw sequencing files are considered. Description Here, we present MetaGeneBank, a standardized database that provides details on sample collection and sequencing, and abundances of genes, microbiota and molecular functions for 4470 raw sequencing files (over 12 TB) collected from 16 studies covering over 10 types of diseases and 14 countries using a unified data-processing pipeline. The incorporation of tools that enable browsing and searching with descriptive attributes, gene sequences, microbiota and functions makes the database user-friendly. We found that the source of specimen contributes more than sequencing centers or platforms to the variations of microbiota. Special attention should be paid when re-analyzing sequencing files from different countries. Conclusions Collectively, MetaGeneBank provides a gateway to utilize the untapped potential of gut metagenomic data in helping fighting against human diseases. With the continuous updating of the database in terms of data volume, data types and sample types, MetaGeneBank would undoubtedly be the benchmarking database in the future in respect of data reuse, and would be valuable in translational science.

The heterogeneity of liver non-parenchymal cells (NPCs) is essential for liver structure and function. However, the current understanding of liver NPCs, especially in different liver diseases, remains incompletely elucidated. Here, a single-cell transcriptome atlas of 171,814 NPCs from healthy and 5 typical liver disease mouse models, including alcoholic liver disease, nonalcoholic steatohepatitis (NASH), drug-induced liver injury, cholestatic, and ischemia-reperfusion liver injury is constructed. The inter- and intra-group heterogeneity of 12 types (and numerous subtypes) of NPCs involving endothelial cells, hepatic stellate cells (HSCs), neutrophils, T cells, and mononuclear phagocytes (MPs) are summarized. A protective subtype of neutrophils characterized by Chil3high is validated and found significantly increasing only in drug-induced and cholestatic liver injury models. Transcriptional regulatory network analysis reveals disease-specific transcriptional reprogramming. Metabolic activity analysis indicates that fibrosis is accompanied by increases in glycolysis and retinol metabolism in activated HSCs and MPs. Moreover, we found that cell-cell interactions between cholangiocytes and immune cells contribute more to cholestatic liver fibrosis compared with NASH, while HSCs are more important for NASH fibrosis. Our atlas, together with an interactive website provides a systematic view of highly heterogeneous NPCs and a valuable resource to better understand pathological mechanisms underlying liver diseases.