The human microbiome is an integral component of the human body and a co-determinant of several health conditions^1,2. However, the extent to which interpersonal relations shape the individual genetic makeup of the microbiome and its transmission within and across populations remains largely unknown^3,4. Here, capitalizing on more than 9,700 human metagenomes and computational strain-level profiling, we detected extensive bacterial strain sharing across individuals (more than 10 million instances) with distinct mother-to-infant, intra-household and intra-population transmission patterns. Mother-to-infant gut microbiome transmission was considerable and stable during infancy (around 50% of the same strains among shared species (strain-sharing rate)) and remained detectable at older ages. By contrast, the transmission of the oral microbiome occurred largely horizontally and was enhanced by the duration of cohabitation. There was substantial strain sharing among cohabiting individuals, with 12% and 32% median strain-sharing rates for the gut and oral microbiomes, and time since cohabitation affected strain sharing more than age or genetics did. Bacterial strain sharing additionally recapitulated host population structures better than species-level profiles did. Finally, distinct taxa appeared as efficient spreaders across transmission modes and were associated with different predicted bacterial phenotypes linked with out-of-host survival capabilities. The extent of microorganism transmission that we describe underscores its relevance in human microbiome studies⁵, especially those on non-infectious, microbiome-associated diseases.

Background: Despite available clinical management strategies, chronic kidney disease (CKD) is associated with severe morbidity and mortality worldwide, which beckons new solutions. Host-microbial interactions with a depletion of Faecalibacterium prausnitzii in CKD are reported. However, the mechanisms about if and how F prausnitzii can be used as a probiotic to treat CKD remains unknown. Methods: We evaluated the microbial compositions in 2 independent CKD populations for any potential probiotic. Next, we investigated if supplementation of such probiotic in a mouse CKD model can restore gut-renal homeostasis as monitored by its effects on suppression on renal inflammation, improvement in gut permeability and renal function. Last, we investigated the molecular mechanisms underlying the probiotic-induced beneficial outcomes. Results: We observed significant depletion of Faecalibacterium in the patients with CKD in both Western (n=283) and Eastern populations (n=75). Supplementation of F prausnitzii to CKD mice reduced renal dysfunction, renal inflammation, and lowered the serum levels of various uremic toxins. These are coupled with improved gut microbial ecology and intestinal integrity. Moreover, we demonstrated that the beneficial effects in kidney induced by F prausnitzii -derived butyrate were through the GPR (G protein-coupled receptor)-43. Conclusions: Using a mouse CKD model, we uncovered a novel beneficial role of F prausnitzii in the restoration of renal function in CKD, which is, at least in part, attributed to the butyrate-mediated GPR-43 signaling in the kidney. Our study provides the necessary foundation to harness the therapeutic potential of F prausnitzii for ameliorating CKD.

Growth retardation of calves is defined as a symptom of impaired growth and development, probably due to growth hormone disorder as well as natural and environmental factors in livestock. The growth-promoting effects of probiotics were determined in 50 growth-retarded growth calves. They were supplied with Bacillus amyloliquefaciens C-1 (Ba, 4 × 10¹⁰CFU/d, n = 16), B. subtilis (Bs, 4 × 10¹⁰CFU/d, n = 18), and negative control (NC, n = 16) for 30 days. Pre- and post-intervention, the growth performance (weight gain rate, feed intake and feed conversion rate) was analyzed, the serum GH, IGH-1 and immunoglobulin levels were assayed, and the fecal microbiota was detected. Calves in Ba and Bs groups demonstrated increased body weight gain, feed intake and GH/IGF-1 levels, as well as a more efficient feed conversion rate, compared with NC group (P < 0.05). Additionally, the abundances of bacteria contributing to the production of energy and SCFAs (short chain fatty acids), including Proteobacteria, Rhodospirillaceae, Campylobacterales, and Butyricimonas were increased compared with NC group (P < 0.05, FDR < 0.1); and the suspected pathogens, which included Anaeroplasma and Acholeplasma were decreased (P < 0.05, FDR < 0.1) in both the Bs and Ba groups. Akkermansia, which is involved in the intestinal mucosal immune response, was increased in Bs group after intervention (P < 0.05, FDR < 0.1), but exhibited no obvious difference in Ba group. The increased bacterial genera in Ba group were Sphaerochaeta and Treponema (P < 0.05, FDR < 0.1). These results indicate that the probiotics B. amyloliquefaciens and B. subtilis exhibited similar therapeutic potential in terms of growth performance by regulating hormones, and improving the intestinal and rumen development in growth-retarded animals.

Psychiatric disorders are a group of complex psychological syndromes with high prevalence. It has been reported that gut microbiota has a dominant influence on the risks of psychiatric disorders through gut microbiota–brain axis. We extended the classic gene set enrichment analysis (GSEA) approach to detect the association between gut microbiota and complex diseases using published genome-wide association study (GWAS) and GWAS of gut microbiota summary data. We applied our approach to real GWAS data sets of five psychiatric disorders, including attention deficiency/hyperactive disorder (ADHD), autism spectrum disorder (AUT), bipolar disorder (BD), schizophrenia (SCZ) and major depressive disorder (MDD). To evaluate the performance of our approach, we also tested the genetic correlations of obesity and type 2 diabetes with gut microbiota. We identified several significant associations between psychiatric disorders and gut microbiota, such as ADHD and genus Desulfovibrio (P = 0.031), order Clostridiales (P = 0.034). For AUT, association signals were observed for genera Bacteroides (P = 0.012) and Desulfovibrio (P = 0.033). Genus Desulfovibrio (P = 0.005) appeared to be associated with BD. For MDD, association signals were observed for genus Desulfovibrio (P = 0.003), order Clostridiales (P = 0.004), family Lachnospiraceae (P = 0.007) and genus Bacteroides (P = 0.007). Genus Desulfovibrio (P = 0.012) and genus Bacteroides (P = 0.038) appeared to be associated with SCZ. Our study results provide novel clues for revealing the roles of gut microbiota in psychiatric disorders. This study also illustrated the good performance of GSEA approach for exploring the relationships between gut microbiota and complex diseases.

Calcium carbonate increases growth, substrate utilization, and acetone-butanol-ethanol (ABE) fermentation byClostridium beijerinckiiNCIMB 8052. Toward an understanding of the basis for these pleiotropic effects, we profiled changes in theC. beijerinckiiNCIMB 8052 proteome that occur in response to the addition of CaCO₃. We observed increases in the levels of different heat shock proteins (GrpE and DnaK), sugar transporters, and proteins involved in DNA synthesis, repair, recombination, and replication. We also noted significant decreases in the levels of proteins involved in metabolism, nucleic acid stabilization, sporulation, oxidative and antibiotic stress responses, and signal transduction. We determined that CaCO₃enhances ABE fermentation due to both its buffering effects and its ability to influence key cellular processes, such as sugar transport, butanol tolerance, and solventogenesis. Moreover, activity assaysin vitrofor select solventogenic enzymes revealed that part of the underpinning for the CaCO₃-mediated increase in the level of ABE fermentation stems from the enhanced activity of these catalysts in the presence of Ca²⁺. Collectively, these proteomic and biochemical studies provide new insights into the multifactorial basis for the stimulation of ABE fermentation and butanol tolerance in the presence of CaCO₃.