Melatonin attenuates microbiota dysbiosis of jejunum in short-term sleep deprived mice.

Our study demonstrated that sleep deprivation resulted in homeostasis disorder of colon. Our study goes deeper into the positive effects of melatonin on small intestinal microbiota disorder caused by sleep deprivation. We successfully established a multiplatform 72 h sleep deprivation mouse model with or without melatonin supplementation, and analyzed the change of small intestinal microbiota using high-throughput sequencing of the 16S rRNA. We found melatonin supplementation suppressed the decrease of plasma melatonin level in sleep deprivation mice. Meanwhile, melatonin supplementation improved significantly the reduction in OTU numbers and the diversity and richness of jejunal microbiota and the abundance of Bacteroidaeae and Prevotellaceae, as well as an increase in the Firmicutes-to-Bacteroidetes ratio and the content of Moraxellaceae and Aeromonadaceae in the jejunum of sleep deprived-mice. Moreover, melatonin supplementation reversed the change of metabolic pathway in sleep deprived-mice, including metabolism, signal transduction mechanisms and transcription etc, which were related to intestinal health. Furthermore, melatonin supplementation inverted the sleep deprivation-induced a decline of anti-inflammatory cytokines (IL-22) and an increase of the ROS and proinflammatory cytokines (IL-17) in jejunum. These findings suggested that melatonin, similar to a probiotics agent, can reverse sleep deprivation-induced small intestinal microbiota disorder by suppressing oxidative stress and inflammation response.

Increasing dietary nitrate has no effect on cancellous bone loss or fecal microbiome in ovariectomized rats.

SCOPE: Studies suggest diets rich in fruit and vegetables reduce bone loss, although the specific compounds responsible are unknown. Substrates for endogenous nitric oxide (NO) production, including organic nitrates and dietary nitrate, may support NO production in age-related conditions, including osteoporosis. We investigated the capability of dietary nitrate to improve NO bioavailability, reduce bone turnover and loss. METHODS AND RESULTS: Six-month-old Sprague Dawley rats [30 ovariectomized (OVX) and 10 sham-operated (sham)] were randomized into three groups: (i) vehicle (water) control, (ii) low-dose nitrate (LDN, 0.1 mmol nitrate/kg bw/day), or (iii) high-dose nitrate (HDN, 1.0 mmol nitrate/kg bw/day) for three weeks. The sham received vehicle. Serum bone turnover markers; bone mass, mineral density, and quality; histomorphometric parameters; and fecal microbiome were examined. Three weeks of LDN or HDN improved NO bioavailability in a dose-dependent manner. OVX resulted in cancellous bone loss, increased bone turnover, and fecal microbiome changes. OVX increased relative abundances of Firmicutes and decreased Bacteroideceae and Alcaligenaceae. Nitrate did not affect the skeleton or fecal microbiome. CONCLUSION: These data indicate that OVX affects the fecal microbiome and that the gut microbiome is associated with bone mass. Three weeks of nitrate supplementation does not slow bone loss or alter the fecal microbiome in OVX.

Clinical and microbiological changes associated with the use of 4 adjunctive systemically administered agents in the treatment of periodontal infections.

The purpose of the present investigation was to assess the effects of periodontal surgery and 4 systemically administered agents, Augmentin, tetracycline, ibuprofen or a placebo on clinical and microbiological parameters of periodontal disease. 98 subjects were monitored at 2-month intervals at 6 sites per tooth for clinical parameters. Subgingival plaque samples were taken from the mesial surface of each tooth at each visit and evaluated for their content of 14 subgingival species using DNA probes and a colony lift method. 40 subjects who exhibited loss of attachment > 2.5 mm at 1 or more sites during longitudinal monitoring were treated using modified Widman flap surgery at sites with probing pocket depth > 4 mm, subgingival scaling at all other sites and were randomly assigned 1 of the 4 agents. Treatment was completed within 30 days during which time the subject took the assigned agent. Overall, subjects exhibited a mean attachment level "gain" of 0.34 +/- 0.10 mm (SEM) and a mean pocket depth reduction of 0.62 +/- 0.09 mm 10 +/- 4 months post-therapy. However, certain subjects in each treatment group showed a poor response. Subjects receiving antibiotics exhibited significantly more attachment level "gain" (0.57 +/- 0.15 mm, SEM) than subjects receiving either ibuprofen or a placebo (0.02 +/- 0.10). The differences between Augmentin and tetracycline groups were not significant, nor were the differences between ibuprofen and placebo. 10 months post-therapy, there was a reduction in the number of sites colonized in any subject group by detectable levels (10(3)) of P. gingivalis. Species showing similar reductions were B. forsythus, P. intermedia and P. micros. Subjects receiving systemically administered antibiotics had a significant increase in the proportion of sites colonized by C. ochracea coupled with a greater decrease in the number of sites colonized by P. gingivalis, B. forsythus, P. intermedia and P. micros post-therapy than subjects not receiving antibiotics. The results of this investigation indicate that adjunctive systemic antibiotics increase periodontal attachment "gain" and decrease the levels of some suspected periodontal pathogens in subjects with evidence of current disease progression.

Human root caries: microbiota in plaque covering sound, carious and arrested carious root surfaces.

The plaque microbiota covering sound or carious root surfaces were studied and compared with that covering arrested root caries lesions. From each of these categories five extracted teeth were examined. The experimental design of the study allowed us to relate the qualitative and quantitative microbial composition to the degree of integrity of the root surface. Plaque was sampled by a newly developed 'mowing' technique. Plaque samples were cultured anaerobically on nonselective Columbia blood agar plates supplemented with 5% hemolyzed human blood and on media selective for Lactobacillus spp. and streptococci of the mutans group. The cultivable microbiota were quantitatively speciated using Rapid ID 32A, Rapid ID 32 Strep, API 20 Strep, API ZYM, and API 50 CH tests and SDS-PAG electrophoresis. Regardless of the state of mineralization, the microbiota on all surfaces resembled marginal plaque associated with gingivitis. In addition to the gram-positive predominant facultative anaerobic genera Streptococcus, Staphylococcus, Lactobacillus and Actinomyces, gram-negative anaerobes, predominantly Bacteroides, Prevotella, Selenomonas, Fusobacterium, Leptotrichia, and Capnocytophaga, showed the highest isolation frequencies. On all surfaces Actinomyces spp. predominated, with streptococci and lactobacilli forming a minor part of the microbiota. With respect to the detected proportions of anaerobes, microaerophiles, Actinomyces naeslundii, Prevotella buccae and Selenomonas dianae, significant differences were observed between the three categories of root surfaces. The total CFU's on both caries-free and caries-active surfaces were significantly higher than on arrested lesions. In general, the results support a polymicrobial etiology for caries initiation on root surfaces, with A. naeslundii, Capnocytophaga spp., and Prevotella spp. making specific contributions to the processes of cementum and dentin breakdown.

Organisms isolated from severe odontogenic soft tissue infections: their sensitivities to cefotetan and seven other antibiotics, and implications for therapy and prophylaxis.

Cefotetan is a new cephamycin antibiotic characterised by excellent B-lactamase stability and anti-anaerobe activity, coupled with a long half life of 3-4 h which permits twice daily dosage. A clinical trial of cefotetan in the treatment of severe oro-facial infections is presented, together with a detailed analysis of the causative organisms and their sensitivities to eight antibiotics. 50/50 patients achieved clinical cure with a treatment regime comprising cefotetan therapy and incision and drainage, with patients being transferred to oral cephradine for the final phase of therapy. Side effects were minimal and there were no instances of relapse. Significant resistance among alpha-haemolytic streptococci and bacteroides organisms to penicillin was observed. The streptococci were resistant due to mechanisms other than beta-lactamase production. In the light of these findings and the reports of other workers it is suggested that penicillin V may no longer be the most appropriate drug for endocarditis prophylaxis, despite the most recent recommendations of the American Heart Association. Furthermore, if penicillin V is used for this purpose, a penicillin free interval of 6-8 weeks may be inadequate before this drug is used. Cefotetan is not suitable for prophylaxis against endocarditis.