RESUMEN
Most animals co-exist with diverse host-associated microbial organisms that often form complex communities varying between individuals, habitats, species and higher taxonomic levels. Factors driving variation in the diversity of host-associated microbes are complex and still poorly understood. Here, we describe the bacterial composition of field-collected Hydra, a freshwater cnidarian that forms stable associations with microbial species in the laboratory and displays complex interactions with components of the microbiota. We sampled Hydra polyps from 21 Central European water bodies and identified bacterial taxa through 16S rRNA sequencing. We asked whether diversity and taxonomic composition of host-associated bacteria depends on sampling location, habitat type, host species or host reproductive mode (sexual vs. asexual). Bacterial diversity was most strongly explained by sampling location, suggesting that the source environment plays an important role in the assembly of bacterial communities associated with Hydra polyps. We also found significant differences between host species in their bacterial composition that partly mirrored variations observed in lab strains. Furthermore, we detected a minor effect of host reproductive mode on bacterial diversity. Overall, our results suggest that extrinsic (habitat identity) factors predict the diversity of host-associated bacterial communities more strongly than intrinsic (species identity) factors, however, only a combination of both factors determines microbiota composition in Hydra.
RESUMEN
Salmonella spp. remains a major public health problem for the whole world. Intestinal epithelial cells serve as an essential component of the innate mucosal immune system to defend against Salmonella infection. A substantial amount of evidence has accumulated that probiotics can regulate interleukin 8 (IL-8) involved in innate immunity. However, the exact effect of probiotics on epithelial IL-8 response to Salmonella infection is not well understood. Therefore, we investigated the action of probiotics on Salmonella-infected Caco-2 cells and its novel mechanisms. Two probiotic strains were examined for Salmonella-induced IL-8 responses and regulating proteins using Caco-2 cell cultures. We demonstrated probiotic, either Lactobacillus rhamnosus GG or Bifidobacterium animalis subsp. lactis DSM10140, administered before Salmonella infection conferred significantly suppressive effect on Salmonella-induced IL-8 responses in Caco-2 cells, either in secreted protein or mRNA, via the PI3K/Akt signal pathway while probiotic administered after infection enhanced Salmonella-induced IL-8 responses via nucleotide-binding oligomerisation domain-containing protein 2 expression in membrane. These findings suggest that the different regulation of probiotics on Salmonella-induced IL-8 responses in Caco-2 cells according to the administered timing supports a rationale for the therapeutic use of probiotics in the treatment of Salmonella colitis and inflammatory bowel disease. This can explain the reported controversial effect of probiotics on these diseases.
Asunto(s)
Bifidobacterium , Lactobacillus , Probióticos/administración & dosificación , Infecciones por Salmonella/inmunología , Salmonella/inmunología , Células CACO-2 , Células Epiteliales/inmunología , Humanos , Inmunidad Innata , Inmunidad Mucosa , Factores Inmunológicos , Interleucina-8/metabolismo , Mucosa Intestinal/inmunología , Proteína Adaptadora de Señalización NOD2/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Infecciones por Salmonella/microbiología , Transducción de SeñalRESUMEN
The aim of this study was to investigate the mechanisms underlying the involvement of gut microbes in body weight gain of high-fat diet-fed obesity-prone (obese) and obesity-resistant (lean) mice. C57BL/6 mice were grouped into an obese group, a lean group and a normal control group. Both obese and lean mice were fed a high-fat diet while normal control mice were fed a normal diet; they were observed for six weeks. The results showed that lean mice had lower serum lipid levels, body fat and weight gain than obese mice. The ATPase, succinate dehydrogenase and malate dehydrogenase activities in liver as well as oxygen expenditure and rectal temperature of lean mice were significantly lower than in obese mice. As compared with obese mice, the absorption of intestinal carbohydrates but not of fats or proteins was significantly attenuated in lean mice. Furthermore, 16S rRNA abundances of faecal Firmicutes and Bacteroidetes were significantly reduced in lean mice. In addition, faecal ß-D-galactosidase activity and short chain fatty acid levels were significantly decreased in lean mice. Expressions of peroxisome proliferator-activated receptor gamma 2 and CCAAT/enhancer binding protein-ß in visceral adipose tissues were significantly downregulated in lean mice as compared with obese mice. Resistance to dyslipidaemia and high-fat diet-induced obesity was mediated by ineffective absorption of intestinal carbohydrates but not of fats or proteins, probably through reducing gut Bacteroidetes and Firmicutes contents and lowering of gut carbohydrate metabolism. The regulation of intestinal carbohydrates instead of fat absorption by gut microbes might be a potential treatment strategy for high-fat diet-induced obesity.