Alterations in Intestinal Microbiota Composition in Mice Treated With Vitamin D3 or Cathelicidin.
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ABSTRACT:
SUBMITTER: Jiang Y
PROVIDER: S-EPMC8732771 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Sex hormone secretion difference is one of the main reasons for sexually dimorphic traits in animals, which affects the dimorphism of the intestinal microbiota; however, their interaction is still unknown. Intestinal mucosa-associated microbiota (MAM) and intestinal luminal content microbiota (LM) belong to two different habitats according to the difference in interactions between bacteria and host intestinal epithelium/nutrients. To clarify the sexually dimorphic characteristics of MAM and LM and their correlation with sex hormones, 12 specific pathogen-free (SPF) Kunming mice from the same nest were fed separately according to sex. After 8 weeks, samples from the male intestinal mucosa group (MM group), the female intestinal mucosa group (FM group), the male intestinal content group (MC group), and the female intestinal content group (FC group) were collected and then, the next-generation sequencing of 16S ribosomal ribonucleic acid (rRNA) gene was performed. Our results showed that the sexual dimorphism of MAM was more obvious than that of LM and the relative abundance of Muribaculaceae, Turicibacter, and Parasutterella was significantly higher in the FM group than in the MM group (p < 0.001, p < 0.05, p < 0.05). Next, we measured the level of serum sex hormones in mice and calculated the correlation coefficient between major bacteria and sex hormones. The results showed that the correlation between MAM and sex hormones was more prominent, and finally, three bacterial genera (Muribaculaceae, Turicibacter, and Parasutterella) were obtained, which could better represent the relationship between sexual dimorphism and sex hormones. The abundance of Parasutterella is positively and negatively correlated with estradiol and testosterone (T), respectively, which may be related to the differences in the metabolism of bile acid and glucose. A decrease in the abundance of Turicibacter is closely related to autism. Our results show that the abundance of Turicibacter is negatively and positively correlated with T and estradiol, respectively, which can provide a hint for the prevalence of male autism. In conclusion, it is proposed in our study that intestinal microbiota is probably the biological basis of physiological and pathological differences due to sex, and intestinal MAM can better represent the sexual dimorphism of mice.
| S-EPMC9659915 | biostudies-literature
Project description:16S rRNA sequencing of human fecal samples has been tremendously successful in identifying microbiome changes associated with both aging and disease. A number of studies have described microbial alterations corresponding to physical frailty and nursing home residence among aging individuals. A gut-muscle axis through which the microbiome influences skeletal muscle growth/function has been hypothesized. However, the microbiome has yet to be examined in sarcopenia. Here, we collected fecal samples of 60 healthy controls (CON) and 27 sarcopenic (Case)/possibly sarcopenic (preCase) individuals and analyzed the intestinal microbiota using 16S rRNA sequencing. We observed an overall reduction in microbial diversity in Case and preCase samples. The genera Lachnospira, Fusicantenibacter, Roseburia, Eubacterium, and Lachnoclostridium-known butyrate producers-were significantly less abundant in Case and preCase subjects while Lactobacillus was more abundant. Functional pathways underrepresented in Case subjects included numerous transporters and phenylalanine, tyrosine, and tryptophan biosynthesis suggesting that protein processing and nutrient transport may be impaired. In contrast, lipopolysaccharide biosynthesis was overrepresented in Case and PreCase subjects suggesting that sarcopenia is associated with a pro-inflammatory metagenome. These analyses demonstrate structural and functional alterations in the intestinal microbiota that may contribute to loss of skeletal muscle mass and function in sarcopenia.
| S-EPMC7907362 | biostudies-literature
Project description:Cathelicidin is strongly expressed in lesional skin in psoriasis and may play an important role as both an antimicrobial peptide and as an autoinflammatory mediator in this chronic skin disease. The mechanism of increased cathelicidin in psoriatic keratinocytes is not known, but recent observations have found that psoriasis has abundant Th17 cells that produce IL-17A and IL-22. We found that human keratinocytes stimulated with supernatants from T cells isolated from lesional psoriatic skin increased expression of cathelicidin when stimulated in the presence of 1,25-dihydroxyvitamin D(3) (1,25D(3)). This increase was signaled through the IL-17RA. In vitro, IL-17A, but not IL-22, enhanced cathelicidin mRNA and peptide expression in keratinocytes dependent on the presence of 1,25D(3). At the same time, coincubation with 1,25D(3) blocked induction of human beta-defensin 2 (HBD2), IL-6, and IL-8, which are other target genes of IL-17A. Act1, an adaptor associated with IL-17RA and essential for IL-17A signaling, mediated cathelicidin induction, as its suppression by small interfering RNA inhibited HBD2 and cathelicidin. Both, 1,25D(3) and IL-17A signaled cathelicidin induction through MEK-ERK. These results suggest that increased IL-17A in psoriatic skin increases cathelicidin through a vitamin D(3)-, Act1-, and MEK-ERK-dependent mechanism. Therapy targeting this cathelicidin-regulating system might be beneficial in patients suffering from psoriasis.
| S-EPMC2655307 | biostudies-literature
Project description:BackgroundThe intestinal barrier integrity is crucial for maintaining intestinal homeostasis, and the mechanisms of intestinal barrier disruption induced by burn injury remain obscure. This study was aimed to investigate the changes of intestinal microbiota and barrier function in burned mice to further comprehend the mechanisms of burn-induced intestinal barrier dysfunction.MethodsSamples were from mice inflicted with 30% total body surface area (TBSA) full-thickness burns. The intestinal permeability, tight junction proteins expressions, zonula occludens-1 (ZO-1) localization, inflammatory cytokines expressions, and short-chain fatty acids (SCFAs) contents were determined. The microbial community was assessed via 16S rDNA Illumina sequencing.ResultsThe intestinal permeability was increased after severe burn injury, peaking at 6 h post-burn, with approximately 20-folds of the control (p < 0.001). The expression of tight junction proteins (ZO-1, occludin, claudin-1, and claudin-2) was significantly altered (p < 0.05). The ZO-1 morphology was dramatically changed following burn injury. The fecal SCFAs' contents (acetate, propionate, butyrate, isobutyrate, and isovalerate) were noticeably declined after burn injury (p < 0.05). The expressions of pro-inflammatory cytokines (interleukin (IL)-1β and IL-6) in ileal mucosa were increased, whereas the expressions of anti-inflammatory cytokines (IL-4 and IL-13) were decreased following burn injury (p < 0.05). In addition, burned mice showed an alteration of intestinal microbial community, such as decreased diversity, reduced Bacteroidetes abundance, and increased Firmicutes abundance.ConclusionsThe severe burn-induced intestinal barrier dysfunction is along with the alterations of microbial community.
| S-EPMC6610819 | biostudies-literature
Project description:Corneal nerve homeostasis is essential for the functional integrity of the ocular surface. Vitamin D deficiency (VDD) and vitamin D receptor knockout (VDR KO) have been found to reduce corneal nerve density in diabetic mice. This is the first study to comprehensively examine the influence of vitamin D on nerve regeneration following corneal epithelial injury in diabetic mice. Corneal nerve regeneration was significantly retarded by diabetes, VDR KO, and VDD, and it was accelerated following topical 1,25 Vit D and 24,25 Vit D administration. Furthermore, topical 1,25 Vit D and 24,25 Vit D increased nerve growth factor, glial cell line-derived neurotropic factor, and neurotropin-3 protein expression, and it increased secretion of GDNF protein from human corneal epithelial cells. CD45+ cells and macrophage numbers were significantly decreased, and vitamin D increased CD45+ cell and macrophage recruitment in these wounded diabetic mouse corneas. The accelerated nerve regeneration observed in these corneas following topical 1,25 Vit D and 24,25 Vit D administration may be related to the vitamin D-stimulated expression, secretion of neurotrophic factors, and recruitment of immune cells.
| S-EPMC10742127 | biostudies-literature
Project description:The gut microbiota is a unique ecosystem of microorganisms interacting with the host through several biochemical mechanisms. The endocannabinoidome (eCBome), a complex signaling system including the endocannabinoid system, approximately 50 receptors and metabolic enzymes, and more than 20 lipid mediators with important physiopathologic functions, modulates gastrointestinal tract function and may mediate host cell-microbe communications there. Germ-free (GF) mice, which lack an intestinal microbiome and so differ drastically from conventionally raised (CR) mice, offer a unique opportunity to explore the eCBome in a microbe-free model and in the presence of a reintroduced functional gut microbiome through fecal microbiota transplant (FMT). We aimed to gain direct evidence for a link between the microbiome and eCBome systems by investigating eCBome alterations in the gut in GF mice before and after FMT. Basal eCBome gene expression and lipid profiles were measured in various segments of the intestine of GF and CR mice at juvenile and adult ages using targeted quantitative PCR transcriptomics and LC-MS/MS lipidomics. GF mice exhibited age-dependent modifications in intestinal eCBome gene expression and lipid mediator levels. FMT from CR donor mice to age-matched GF male mice reversed several of these alterations, particularly in the ileum and jejunum, after only 1 week, demonstrating that the gut microbiome directly impacts the host eCBome and providing a cause-effect relationship between the presence or absence of intestinal microbes and eCBome signaling. These results open the way to new studies investigating the mechanisms through which intestinal microorganisms exploit eCBome signaling to exert some of their physiopathologic functions.
| S-EPMC6939599 | biostudies-literature
Project description:BackgroundResveratrol (RSV) plays a vital role in alleviating various stresses and improving intestinal health. The current study was conducted to explore whether RSV alleviates weaning stress through improving gut health in a weaning mouse model. Forty 21-day-old weaned mice were randomly assigned to a control group without RSV treatment and three treatment groups with 10, 20, and 50 mg/kg RSV for 28 days.ResultsThe results showed that RSV at a dose of 20 mg/kg improved total body weight, intestinal morphology (villus length and the ratio of villus length to crypt depth), and the levels of intestinal barrier proteins (claudin-1 and occludin), but had little effect on the food intake, crypt depth, and serum free amino acids of mice. Compared with the control group, mice supplemented with RSV had decreased mRNA expression of genes related to inflammatory cytokines (IL-6 and IL-1β), but increased mRNA expression of genes related to host defense peptides (Defa3, Defa5, Defa20, and Lyz) and short-chain fatty acids (SCFAs) production (propionic acid, isobutyric acid, butyric acid, and isovaleric acid). In addition, 16S rRNA sequencing results showed that RSV supplementation increased the richness indices of intestinal microbiota (Chao, ACE) and shaped the composition of intestinal microbiota (e.g., increased β-diversity of intestinal microbiota community). Meanwhile, RSV supplementation increased genes of Butyricicoccus, Ruminococcus_1, and Roseburia, which are producers of SCFAs. Furthermore, RSV supplementation significantly influenced the metabolism of intestinal microbiota, namely, amino acids metabolism, lipid metabolism, and defense mechanisms.ConclusionRSV can improve growth performance and intestinal morphology in weaning mice, possibly through improving gut immune response and microbiota function.
| S-EPMC8446547 | biostudies-literature
Project description:Tributyrin (TB) is a butyric acid precursor and has a key role in anti-inflammatory and intestinal barrier repair effects by slowly releasing butyric acid. However, its roles in gut microbiota disorder caused by antibiotics remain unclear. Herein, we established an intestinal microbiota disorder model using ceftriaxone sodium via gavage to investigate the effects of different TB doses for restoring gut microbiota and intestinal injury. First, we divided C57BL/6 male mice into two groups: control (NC, n = 8) and experimental (ABx, n = 24) groups, receiving gavage with 0.2 mL normal saline and 400 mg/mL ceftriaxone sodium solution for 7 d (twice a day and the intermediate interval was 6 h), respectively. Then, mice in the ABx group were randomly split into three groups: model (M, 0.2 mL normal saline), low TB group (TL, 0.3 g/kg BW), and high TB group (TH, 3 g/kg BW) for 11 d. We found that TB supplementation alleviated antibiotics-induced weight loss, diarrhea, and intestinal tissue damage. The 16S rRNA sequence analysis showed that TB intervention increased the α diversity of intestinal flora, increased potential short-chain fatty acids (SCFAs)-producing bacteria (such as Muribaculaceae and Bifidobacterium), and inhibited the relative abundance of potentially pathogenic bacteria (such as Bacteroidetes and Enterococcus) compared to the M group. TB supplementation reversed the reduction in SCFAs production in antibiotic-treated mice. Additionally, TB downregulated the levels of serum LPS and zonulin, TNF-α, IL-6, IL-1β and NLRP3 inflammasome-related factors in intestinal tissue and upregulated tight junction proteins (such as ZO-1 and Occludin) and MUC2. Overall, the adjustment ability of low-dose TB to the above indexes was stronger than high-dose TB. In conclusion, TB can restore the dysbiosis of gut microbiota, increase SCFAs, suppress inflammation, and ameliorate antibiotic-induced intestinal damage, indicating that TB might be a potential gut microbiota modulator.
| S-EPMC10389721 | biostudies-literature
Project description:Psoriasis is a chronic, inflammatory skin disease. Although the precise etiology of psoriasis remains unclear, gut-microbiota axis might play a role in the pathogenesis of the disease. Here we investigated whether the composition of microbiota in the intestine and skin is altered in the imiquimod (IMQ)-treated mouse model of psoriasis. Topical application of IMQ to back skin caused significant changes in the composition of microbiota in the intestine and skin of IMQ-treated mice compared to control mice. The LEfSe algorithm identified the species Staphylococcus lentus as potential skin microbial marker for IMQ group. Furthermore, there were correlations for several microbes between the intestine and skin, suggesting a role of skin-gut-microbiota in IMQ-treated mice. Levels of succinic acid and lactic acid in feces from IMQ-treated mice were significantly higher than control mice. Moreover, the predictive functional analysis of the microbiota in the intestine and skin showed that IMQ caused alterations in several KEGG pathways. In conclusion, the current data indicated that topical application with IMQ to skin alters the composition of the microbiota in the gut and skin of host. It is likely that skin-gut microbiota axis plays a role in pathogenesis of psoriasis.
| S-EPMC8163751 | biostudies-literature
Project description:To date, only one study has reported changes in the gut microbiome of an ultramarathon runner before and after competing in the race. Herein we aimed to investigate changes in intestinal microbiota in nine ultramarathon runners. Eight of the nine participants ran 96.102 km (up 8062 m, down 6983 km) and one ran 99.12 km (up 8448 m, down 7369 m) within 38-44 h. Intestinal microbiota alterations were examined at three timepoints: before (Pre), after (Post), and 10 days after (Recovery) the race. The α- and β-diversity of intestinal microbiota were unaffected by the race. Six of the nine participants showed the B-type enterotype, while the remaining three showed the P-type enterotype; however, significant difference between enterotypes was not observed in the influence of the ultramarathon on intestinal microbiota. The abundance of mean Faecalibacterium prausnitzii, was significantly decreased from 2.9% (Pre) to 1.6% (Post), as well as other three butyrate producing bacteria. One participant with the largest decrease in F. prausnitzii abundance (- 85.7%) reported sluggishness and shallow sleep from Post to Recovery. Our findings revealed that the abundance of butyrate-producing bacteria is decreased in ultramarathon runners, which consequently decreases butyrate levels in the intestine and affects host immune function.
| S-EPMC9050700 | biostudies-literature