ABSTRACT
OBJECTIVE Alzheimer's disease(AD)is a progressive neurological disease.Given the important role of gut microbiota composition in AD pathology,the observed perturbation in the microbiota composition and diversity may serve as the mechanisms underlying age-dependent APP/PS1/tau triple-transgenic mouse(3×Tg-AD)mice amyloid deposition and memory deficits.Here-in,we intended to investigate the gut microbiota and as-sessed its relationship with the triggering and develop-ment of cognitive impairment of AD.METHODS This study involves the comparative assessment of spatial learning,amyloid β-protein(Aβ)accumulation,and fecal microbiota alterations in 3×Tg-AD mice from three age groups:AD asymptomatic stage(3 m),presymptomatic stage(6 m),and the symptomatic stage of AD(9 m).RE-SULTS We demonstrate that spatial memory deficits,brain Aβ accumulation,and weight gain in 3×Tg-AD mice gradually appear after 6 months of age.However,the total gut bacterial counts underwent changes from 3 to 6 months of age and were further altered at 9 months of age.Importantly,changes in gut bacteria abundance of Desulfobacterota and Actinobacteriota phylain 6-month-old mice preceded apparent spatial memory deficits.CONCLUSION Changes in the gut microbial community are one of the mechanisms of early AD pathology.
ABSTRACT
Objective@#To investigate the influences of antibiotic-induced gut microbiota dysbiosis on Mycoplasma pneumoniae (Mp) airway infection.@*Methods@#C57BL/6J mice were treated with vancomycin and gentamicin for 21 d by oral delivery and then intranasally infected with Mp. Quantitative real-time PCR (qPCR) was performed to detect five major phyla of gut microbiota in mouse fecal specimens before and after antibiotic treatment and the loads of Mp in lung tissues on 3 d and 7 d after infection. Pathological changes in lung tissues were evaluated with HE staining. IFN-γ and IL-4 secreted by spleen CD4+ T cells and CD8+ T cells were analyzed by flow cytometry. Mp-specific IgM and IgG in mouse serum samples were measured by indirect enzyme-linked immunosorbent assay (ELISA).@*Results@#Vancomycin and gentamicin treatment significantly reduced the number of Bacteroidetes in mouse feces, but increased the amount of Firmicutes. Meanwhile, the numbers of δ, γ-Proteobacteria, Actinomycetes and Tenericutes also changed. These antibiotic-induced gut microbiota alterations in mice with Mp infection increased the loads of Mp in lung tissues and the pathological scores of lung tissue inflammation on 3 d and 7 d after infection, and reduced the number of IFN-γ-secreting spleen CD4+ T lymphocytes on 7 d.@*Conclusions@#Antibiotic-induced gut microbiota dysbiosis aggravated Mp airway infection.
ABSTRACT
Objective To investigate the influences of antibiotic-induced gut microbiota dysbiosis on Mycoplasma pneumoniae (Mp) airway infection. Methods C57BL/6J mice were treated with vancomy-cin and gentamicin for 21 d by oral delivery and then intranasally infected with Mp. Quantitative real-time PCR ( qPCR) was performed to detect five major phyla of gut microbiota in mouse fecal specimens before and after antibiotic treatment and the loads of Mp in lung tissues on 3 d and 7 d after infection. Pathological changes in lung tissues were evaluated with HE staining. IFN-γ and IL-4 secreted by spleen CD4+ T cells and CD8+ T cells were analyzed by flow cytometry. Mp-specific IgM and IgG in mouse serum samples were measured by indirect enzyme-linked immunosorbent assay (ELISA). Results Vancomycin and gentamicin treatment significantly reduced the number of Bacteroidetes in mouse feces, but increased the amount of Fir-micutes. Meanwhile, the numbers of δ, γ-Proteobacteria, Actinomycetes and Tenericutes also changed. These antibiotic-induced gut microbiota alterations in mice with Mp infection increased the loads of Mp in lung tissues and the pathological scores of lung tissue inflammation on 3 d and 7 d after infection, and re-duced the number of IFN-γ-secreting spleen CD4+T lymphocytes on 7 d. Conclusions Antibiotic-induced gut microbiota dysbiosis aggravated Mp airway infection.
ABSTRACT
Gut microbiota is involved in the physiological,biochemical and pathological processes of the body.It could participate in the immunoregulation and the development of enteric nervous system,prevent the invasion of pathogens,maintain normal bowel movement and inhibit the occurrence of tumor.Gut microbiota dysbiosis may also cause many diseases,such as inflammatory bowel disease,obesity and diabetes.A variety of diseases can affect gut microbiota with different ways.In addition,remote organs play a counteractive rule to gut microbiota.Maintaining the balance of the bacteria sets different requirements in different disease processes.This paper reviewed the advanced progression of gut microbiota dysbiosis after cholecystectomy and provided a new therapeutic target for gallbladder diseases.
ABSTRACT
Objective: The aim of this study was to explore the pharmacokinetics of ginsenoside Rg3 and its deglycosylated metabolite, ginsenoside Rh2 in lincomycin-induced gut microbiota dysbiosis rats after ig administration of ginsenoside Rg3. Methods: An LC-MS/MS analytical method was developed and validated to detect ginsenoside Rg3 and Rh2 in plasma of rats. The method was validated by specificity, linearity, lower limits of quantification (LLOQ), precision, accuracy, matrix effect, recovery, and stability. Lincomycin (orally, 5 000 mg/kg, 7 d) was selected to induce gut microbiota dysbiosis. The fecal moisture contents and the β-D-glucosidase activity were also assessed in this study. And the plasma samples were collected and analyzed after ig administration of ginsenoside Rg3 (20 mg/kg). Results: The results indicated that this method could be used for the determination of the concentration of ginsenoside Rg3 and Rh2 in plasma of rats. The fecal moisture content in rats treated with lincomycin was significantly increased (P < 0.01) and the β-D-glucosidase activity was decreased (P < 0.01) compared with the control rats. The AUC0~∞ and Cmax in gut microbiota dysbiosis rats were increased, while the AUC0~t and Cmax of its active metabolite, ginsenoside Rh2 were significantly decreased (P < 0.01) compared with normal rats. Conclusion: The pharmacokinetic profile of ginsenoside Rg3 and Rh2 is changed in gut microbiota dysbiosis rats, which partly relates to the decreased β-D-glucosidase activity.
ABSTRACT
@#Gut microbiota-mediated deglycosylationplays an important role in the metabolism of ginsenoside Rb1. Thus, a lincomycin-induced gut microbiota dysbiosis rat model was selected to explored the pharmacokinetics and deglycosylation metabolism of ginsenoside Rb1. An UPLC-MS/MS analytical method was developed to detect ginsenoside Rb1 and its deglycosylated metabolite, Rd in rat plasma. The triple quadruple mass spectrometer was set in negative electrospray ionization mode by multiple reaction monitoring. The method was validated to meet the requirements of biological applications, by evaluating specificity, linearity, lower limits of quantification(LLOQ), precision, accuracy, matrix effect, recovery and stability. Gut microbiota dysbiosis rats were induced by oral administration of lincomycin(5 000 mg/kg)for 7 continuous days. The in vitro and in vivo results reveal that the reduced β-D-glucosidase activity significantly decreases the Rd formation rate in lincomycin-induced gut microbiota dysbiosis rats, leading to the pharmacokinetic alteration of ginsenoside Rb1 and Rd in gut microbiota dysbiosis rats.