ObjectiveCerebral amyloidosis and severe tauopathy in the brain are key pathological features of Alzheimer’s disease (AD). Despite a strong influence of the intestinal microbiota on AD, the causal relationship between the gut microbiota and AD pathophysiology is still elusive.DesignUsing a recently developed AD-like pathology with amyloid and neurofibrillary tangles (ADLPAPT) transgenic mouse model of AD, which shows amyloid plaques, neurofibrillary tangles and reactive gliosis in their brains along with memory deficits, we examined the impact of the gut microbiota on AD pathogenesis.ResultsComposition of the gut microbiota in ADLPAPT mice differed from that of healthy wild-type (WT) mice. Besides, ADLPAPT mice showed a loss of epithelial barrier integrity and chronic intestinal and systemic inflammation. Both frequent transfer and transplantation of the faecal microbiota from WT mice into ADLPAPT mice ameliorated the formation of amyloid β plaques and neurofibrillary tangles, glial reactivity and cognitive impairment. Additionally, the faecal microbiota transfer reversed abnormalities in the colonic expression of genes related to intestinal macrophage activity and the circulating blood inflammatory monocytes in the ADLPAPT recipient mice.ConclusionThese results indicate that microbiota-mediated intestinal and systemic immune aberrations contribute to the pathogenesis of AD in ADLPAPT mice, providing new insights into the relationship between the gut (colonic gene expression, gut permeability), blood (blood immune cell population) and brain (pathology) axis and AD (memory deficits). Thus, restoring gut microbial homeostasis may have beneficial effects on AD treatment.

Background Our understanding of the gut microbiota of animals is largely based on studies of mammals. To better understand the evolutionary basis of symbiotic relationships between animal hosts and indigenous microbes, it is necessary to investigate the gut microbiota of non-mammalian vertebrate species. In particular, fish have the highest species diversity among groups of vertebrates, with approximately 33,000 species. In this study, we comprehensively characterized gut bacterial communities in fish. Results We analyzed 227 individual fish representing 14 orders, 42 families, 79 genera, and 85 species. The fish gut microbiota was dominated by Proteobacteria (51.7%) and Firmicutes (13.5%), different from the dominant taxa reported in terrestrial vertebrates (Firmicutes and Bacteroidetes). The gut microbial community in fish was more strongly shaped by host habitat than by host taxonomy or trophic level. Using a machine learning approach trained on the microbial community composition or predicted functional profiles, we found that the host habitat exhibited the highest classification accuracy. Principal coordinate analysis revealed that the gut bacterial community of fish differs significantly from those of other vertebrate classes (reptiles, birds, and mammals). Conclusions Collectively, these data provide a reference for future studies of the gut microbiome of aquatic animals as well as insights into the relationship between fish and their gut bacteria, including the key role of host habitat and the distinct compositions in comparison with those of mammals, reptiles, and birds.

Abnormalities in the human microbiota are associated with the etiology of allergic diseases. Although disease site-specific microbiota may be associated with disease pathophysiology, the role of the nasal microbiota is unclear. We sought to characterize the microbiota of the site of allergic rhinitis, the inferior turbinate, in subjects with allergic rhinitis ( = 20) and healthy controls ( = 12) and to examine the relationship of mucosal microbiota with disease occurrence, sensitized allergen number, and allergen-specific and total IgE levels. Microbial dysbiosis correlated significantly with total IgE levels representing combined allergic responses but not with disease occurrence, the number of sensitized allergens, or house dust mite allergen-specific IgE levels. Compared to the populations in individuals with low total IgE levels (group IgE), low microbial biodiversity with a high relative abundance of phylum () and a low relative abundance of phylum () was observed in individuals with high total serum IgE levels (group IgE). Phylogeny-based microbial functional potential predicted by the 16S rRNA gene indicated an increase in signal transduction-related genes and a decrease in energy metabolism-related genes in group IgE as shown in the microbial features with atopic and/or inflammatory diseases. Thus, dysbiosis of the inferior turbinate mucosa microbiota, particularly an increase in and a decrease in, is linked to high total IgE levels in allergic rhinitis, suggesting that inferior turbinate microbiota may be affected by accumulated allergic responses against sensitized allergens and that site-specific microbial alterations play a potential role in disease pathophysiology.

A halophilic archaeal strain, designated CBA1105(T), was isolated from non-purified solar salt. Strain CBA1105(T) was found to have three 16S rRNA genes, rrnA, rrnB and rrnC; similarities between the 16S rRNA gene sequences were 99.5-99.7 %. The phylogenetic analysis of the 16S rRNA gene sequences showed that strain CBA1105(T) forms a distinct clade with the strains of the closely related genera, Halorientalis and Halorhabdus, with similarities of 94.2 % and 93.9-94.2 %, respectively. Multilocus sequence analysis confirmed that strain CBA1105(T) is closely related to the genus Halorhabdus or Halorientalis. Growth of the strain was observed in 15-30 % NaCl (w/v; optimum 20 %), at 30-45 °C (optimum 37 °C) and pH 7.0-8.0 (optimum pH 7.0) and with 0-0.5 M MgCl2·6H2O (optimum 0.05-0.2 M). The cells of the strain were observed to be Gram-stain negative and pleomorphic with coccoid or ovoid-shape. The cells lysed in distilled water. Tweens 20, 40 and 80 were found to be hydrolysed but starch, casein and gelatine were not. The cells were unable to reduce nitrate under aerobic conditions. Assays for indole formation and urease activity were negative and no growth was observed under anaerobic conditions. Cells were found to be able to utilize L-glutamate, D-glucose, L-maltose, D-mannose and sucrose as sole carbon sources. The polar lipids were identified as phosphatidylglycerol, phosphatidylglycerol phosphate methyl ester, unidentified glycolipids and an unidentified phospholipid. The G+C content of strain CBA1105(T) was determined to be 66.0 mol%. The phenotypic, chemotaxonomic and phylogenetic properties suggest that the strain represents a novel species of a novel genus within the family Halobacteriaceae, for which the name Halapricum salinum is proposed with CBA1105(T) (= KCTC 4202(T) = JCM 19729(T)) as the type strain.

Castration of young males is widely used in the cattle industry to improve meat quality, but the mechanism linking hypogonadism and host metabolism is not clear. Here, we use metataxonomic and metabolomic approaches to evaluate the intestinal microbiota and host metabolism in male, castrated male (CtM), and female cattle. After pubescence, the CtM cattle harbor distinct ileal microbiota dominated by the family Peptostreptococcaceae and exhibit distinct serum and muscle amino acid profiles (i.e., highly abundant branched-chain amino acids), with increased extra-and intramuscular fat storage. We also evaluate the causative factor(s) that underpin the alteration of the intestinal microbiota and host metabolic phenotype in response to hypogonadism. Castration of male mice phenocopies both the intestinal microbial alterations and obese-prone metabolism observed in cattle. Antibiotic treatment and fecal microbiota transplantation experiments in a mouse model confirm that the intestinal microbial alterations associated with hypogonadism are a key contributor to the obese phenotype in the CtM animals. Collectively, targeting the gut microbiota is a potential therapeutic strategy for the treatment of both hypogonadism and obesity.