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Metabolism, microflora effects, and genotoxicity in haloacetic acid-treated cultures of rat cecal microbiota.

Haloacetic acids are by-products of drinking water disinfection. Several compounds in this class are genotoxic and have been identified as rodent hepatocarcinogens. Enzymes produced by the normal intestinal bacteria can transform some promutagens and procarcinogens to their biologically active forms. The present study was designed to investigate the influence of the cecal microbiota on the mutagenicity of haloacetic acids, and to look at changes in the microbiota populations and enzyme activities associated with exposure to haloacetic acids. PYG medium containing 1 mg/ml of monochloroacetic (MCA), monobromoacetic (MBA), dichloroacetic (DCA), dibromoacetic (DBA), trichloroacetic (TCA), tribromoacetic (TBA), or bromochloroacetic (BCA) acid was inoculated with rat cecal homogenate and incubated anaerobically at 37 degrees C. Growth curves were performed with enumeration of the microflora populations on selective media. Mutagenicity in a Salmonella microsuspension bioassay was determined after incubation for various lengths of time, with or without the cecal microbiota. At 15 h of incubation, enzyme assays determined the activities for beta-glucuronidase, beta-galactosidase, beta-glucosidase, azoreductase, nitroreductase, dechlorinase, and dehydrochlorinase. The haloacetic acids, with the exception of BCA, were toxic to the cecal microbiota, and especially to the enterococci. DBA, TBA, and BCA were mutagenic in the microsuspension assay, but the presence of the intestinal flora did not significantly alter the mutagenicity. BCA increased the activities of several enzymes, and therefore has the potential to affect the biotransformation of co-exposed compounds.

Acetates↗

Probiotic intervention in the first months of life: short-term effects on gastrointestinal symptoms and long-term effects on gut microbiota.

OBJECTIVES: To determine whether probiotics administered for 6 months postnatally affect gastrointestinal symptoms, crying and the compositional development of the gut microbiota through infancy. METHODS: The study comprised of 132 newborns whose mothers were randomized to receive placebo or Lactobacillus rhamnosus GG (ATCC 53103) before delivery. The treatments of mothers/infants continued for 6 months postnatally. A specific symptom chart was used to monitor gastrointestinal symptoms and infant's crying during the 7th and the 12th weeks of life. Fluorescent in situ hybridization was used to establish the Bifidobacterium, Lactobacillus/Enterococcus, Bacteroides and Clostridium counts in fecal samples at 6, 12, 18 and 24 months of age. RESULTS: Numbers of different types of stools, vomits and crying time were comparable between the groups during the 7th and the 12th weeks of life. Dominant microbiota consisted of bifidobacteria throughout the study. At 6 months, there were less clostridia in faeces in the placebo compared with the probiotic group (P = 0.026), whereas after long-term follow-up at 2 years, there were less lactobacilli/enterococci and clostridia in faeces in the probiotic group than in the placebo group (P = 0.011 and P = 0.032, respectively), reflecting the impact of clostridia as a marker of microbiota succession in healthy infants. CONCLUSIONS: Probiotic administration in the first months of life was well tolerated and did not significantly interfere with long-term composition or quantity of gut microbiota.

Adult↗

Influence of bacteria from the duodenal microbiota of patients with symptomatic giardiasis on the pathogenicity of Giardia duodenalis in gnotoxenic mice.

Recent studies have shown that the intestinal microbiota is essential for the pathogenicity but not for the multiplication of Giardia duodenalis in the intestinal lumen. The microbial components responsible for this phenomenon are not known. Twenty-eight facultative and three strictly anaerobic micro-organisms were isolated from the dominant duodenal microbiota of five patients with symptomatic giardiasis. The bacterial combinations from each patient were associated with groups (GN) of germ-free mice. Five days after the association, when their faecal populations ranged from 10(7) to 10(9) cfu/g, all groups were inoculated intragastrically with 10(5) viable trophozoites of G. duodenalis strain BT6. Two groups of germ-free (GF) and conventional (CV1) mice were also infected. Gnotobiotic animals were killed 10 days after infection and GF and CV1 animals were killed 10, 20 and 30 days after infection. More marked pathological alterations were detected in CV1 mice when compared with GF animals. Gnotobiotic animals showed intermediate pathological alterations between CV1 and GF mice. The CV1 and GF groups became infected by day 3 and faecal cyst levels were similar in both groups throughout the experiment. Total and G. duodenalis-specific IgA levels in the intestinal fluid and G. duodenalis-specific IgM and IgG levels in the serum increased during the infection and were higher in CV1 animals at all times tested when compared with GF mice. The present results confirm the stimulatory activity of the intestinal microbiota on the pathogenicity of G. duodenalis, and some combinations of microbial components of the dominant duodenal ecosystem from patients with symptomatic giardiasis can partially develop this function. However, none of these combinations was able to stimulate the protozoan pathogenicity in the same manner as the entire intestinal microbiota.

Animals↗

Detection of potentially novel bacterial components of the human skin microbiota using culture-independent molecular profiling.

Although the micro-organisms forming the cutaneous microbiota are considered to play important roles in the modification and prevention of skin diseases, a comprehensive analysis of their composition has not yet been carried out because of difficulties in determining yet-to-be-cultured micro-organisms in the samples. Swab-scrubbed forehead skin samples of five healthy volunteers were analysed by profiling 16S rRNA genes, as well as by conventional culture methods, to provide a profile of the cutaneous microbiota that included yet-to-be-cultured bacteria from normal human skin. Cluster analyses of the 16S rRNA gene sequences indicated a marked increase in diversity compared with that derived from the culture methods. Nineteen previously recognized species and 13 novel phylotypes were obtained from the analysis of 416 clones. In addition to well-known bacteria such as Staphylococcus epidermidis and Propionibacterium acnes, phylotype A, the 16S rRNA gene of which is 97 % similar to that of Methylophilus methylotrophus, was detected in three of the five samples, in one of which it was the predominant clone. Culture-independent genetic profiling of 16S rRNA genes for detecting human cutaneous microbiota has allowed us to detect potentially novel components of the cutaneous microbiota in humans.

Bacteria↗

Comparison among fecal secondary bile acid levels, fecal microbiota and Clostridium scindens cell numbers in Japanese.

Bile acid 7alpha-dehydroxylation by intestinal bacteria, which converts cholic acid and chenodeoxycholic acid to deoxycholic acid (DCA) and lithocholic acid (LCA), respectively, is an important function in the human intestine. Clostridium scindens is one of the most important bacterial species for bile acid 7alpha-dehydroxylation because C. scindens has high levels of bile acid 7alpha-dehydroxylating activity. We quantified C. scindens and secondary bile acids, DCA and LCA, in fecal samples from 40 healthy Japanese and investigated their correlation. Moreover, we used terminal restriction fragment length polymorphism (T-RFLP) analysis to investigate the effect of fecal microbiota on secondary bile acid levels. There was no correlation between C. scindens and secondary bile acid in fecal samples. On the other hand, T-RFLP analysis demonstrated that fecal microbiota associated with high levels of DCA were different from those associated with low levels of DCA, and furthermore that fecal microbiota in the elderly (over 72 years) were significantly different from those in younger adults (under 55 years). These results suggest that intestinal microbiota have a stronger effect on DCA level than does the number of C. scindens cells.

Adult↗

Microbiota of health, gingivitis, and initial periodontitis.

This study compared the subgingival microbiota in periodontal health, gingivitis and initial periodontitis using predominant culture and a DNA probe, checkerboard hybridization method. 56 healthy adult subjects with minimal periodontal attachment loss were clinically monitored at 3-month intervals for 12 months. More sites demonstrated small increments of attachment loss than attachment gain over the monitoring period. Sites, from 17 subjects, showing > or = 1.5 mm periodontal attachment loss during monitoring were sampled as active lesions for microbial analysis. Twelve subjects demonstrated interproximal lesions, and 5 subjects had attachment loss at buccal sites (recession). Cultural studies identified Bacteroides forsythus, Campylobacter rectus, and Selenomonas noxia as the predominant species associated with active interproximal lesions (9 subjects), whereas Actinomyces naeslundii, and Streptococcus oralis, were the dominant species colonizing buccal active sites. A. naeslundii, Campylobacter gracilis, and B. forsythus (at lower levels than active sites) were the dominant species cultured from gingivitis (10 subjects). Health-associated species (10 subjects) included Streptococcus oralis, A. naeslundii, and Actinomyces gerencseriae. DNA probe data identified higher mean levels of B. forsythus and C. rectus with active (7 subjects) compared to inactive periodontitis sites. Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans were detected infrequently. Cluster analysis of the cultural microbiota grouped 8/9 active interproximal lesions in one subcluster characterized by a mostly gram-negative microbiota, including B. forsythus and C. rectus. The data suggest that B. forsythus C. rectus and S. noxia were major species characterizing sites converting from periodontal health to disease. The differences in location and microbiota of interproximal and buccal active sites suggested that different mechanisms may be involved in increased attachment loss.

Adult↗

Oral microbiota in smokers and non-smokers in natural and experimentally-induced gingivitis.

The present study primarily aimed at investigating the oral microbiota in smokers and non-smokers with established gingivitis and monitoring its composition during experimental gingivitis. Secondly, it aimed at examining whether the composition of the microbiota is associated with different levels of gingival inflammation during this experimental gingivitis trial. For this purpose, 25 non-dental university students with gingivitis were recruited. 11 subjects were smokers and 14 were non-smokers. After achieving gingival health, they entered a 14-day experimental gingivitis trial. Plaque and bleeding were assessed before entering into the study (intake), at day 0, day 5 and at day 14 of the experiment. Microbiological samples from mucosal sites and dental plaque (taken at intake, day 0, and day 14) were analysed for the presence of Actinomyces species, Actinobacillus actinomycetemcomitans, Bacteroides forsythus, Campylobacter rectus, Fusobacterium nucleatum, Peptostreptococcus micros, Porphyromonas gingivalis, Prevotella intermedia and Streptococcus species. At day 14 of the experimental period, the level of plaque formation was not different between smokers and non-smokers, but bleeding scores were lower in smokers than in non-smokers (15% and 30% respectively, p=0.01). The change from natural gingivitis to a state of gingival health and a subsequent change from gingival health to experimentally induced gingivitis was accompanied by quantitative alterations in the cultivable microbiota in both groups. Changes were most prominent in the transition from gingival health to experimental gingivitis and were found in dental plaque for Actinomyces species, C. rectus, F. nucleatum, and P. intermedia. Within the group of non-smokers, a distinction was made between subjects with a 'weak' or 'strong' inflammatory response. No relationship with a single bacterial species could be established which would likely explain the differences in levels of inflammation. It is concluded that differences in response to experimental gingivitis are not caused by major differences in the composition of the oral microbiota.

Actinomyces↗

Improved understanding of the bacterial vaginal microbiota of women before and after probiotic instillation.

The vaginal bacterial microbiota of 19 premenopausal women was examined by PCR-denaturing gradient gel electrophoresis (DGGE) and sequencing of the V2-V3 region of the 16S rRNA gene. Ten of the women were studied further to investigate the effect and persistence of vaginally inserted capsules containing viable lactobacilli. PCR-DGGE indicated that most subjects had a microbiota represented by one to three dominant DNA fragments. Analysis of these fragments revealed that 79% of the women possessed sequences with high levels of similarity to Lactobacillus species sequences. Sequences homologous to Lactobacillus iners sequences were the most common and were detected in 42% of the women tested. Alteration of the vaginal microbiota could be detected by PCR-DGGE in several women after the instillation of lactobacilli. Additionally, randomly amplified polymorphic DNA analysis of lactobacilli isolated from selective media demonstrated that the exogenous strains could be detected for up to 21 days in some subjects. This study demonstrates that non-culture-based techniques, such as PCR-DGGE, are useful adjuncts for studies of the vaginal microbiota.

Adult↗

Comparison between cultured small-intestinal and fecal microbiotas in beagle dogs.

The microbiota of the small intestine is poorly known because of difficulties in sampling. In this study, we examined whether the organisms cultured from the jejunum and feces resemble each other. Small-intestinal fluid samples were collected from 22 beagle dogs with a permanent jejunal fistula in parallel with fecal samples. In addition, corresponding samples from seven of the dogs were collected during a 4-week period (days 4, 10, 14, and 28) to examine the stability of the microbiota. In the jejunal samples, aerobic/facultative and anaerobic bacteria were equally represented, whereas anaerobes dominated in the fecal samples. Despite lower numbers of bacteria in the jejunum (range, 10(2) to 10(6) CFU/g) than in feces (range, 10(8) to 10(11) CFU/g), some microbial groups were more prevalent in the small intestine: staphylococci, 64% versus 36%; nonfermentative gram-negative rods, 27% versus 9%; and yeasts, 27% versus 5%, respectively. In contrast, part of the fecal dominant microbiota (bile-resistant Bacteroides spp., Clostridium hiranonis-like organisms, and lactobacilli) was practically absent in the jejunum. Many species were seldom isolated simultaneously from both sample types, regardless of their overall prevalence. In conclusion, the small intestine contains a few bacterial species at a time with vastly fluctuating counts, opposite to the results obtained for the colon, where the major bacterial groups remain relatively constant over time. Qualitative and quantitative differences between the corresponding jejunal and fecal samples indicate the inability of fecal samples to represent the microbiotas present in the upper gut.

Animals↗

Effects of Lactococcus lactis on composition of intestinal microbiota: role of nisin.

This study examined the ability of (i) pure nisin, (ii) nisin-producing Lactococcus lactis strain CHCC5826, and (iii) the non-nisin-producing L. lactis strain CHCH2862 to affect the composition of the intestinal microbiota of human flora-associated rats. The presence of both the nisin-producing and the non-nisin-producing L. lactis strains significantly increased the number of Bifidobacterium cells in fecal samples during the first 8 days but decreased the number of enterococci/streptococci in duodenum, ileum, cecum, and colon samples as detected by selective cultivation. No significant changes in the rat fecal microbiota were observed after dosage with nisin. Pearson cluster analysis of denaturing gradient gel electrophoresis profiles of the 16S rRNA genes present in the fecal microbial population revealed that the microbiota of animals dosed with either of the two L. lactis strains were different from that of control animals dosed with saline. However, profiles of the microbiota from animals dosed with nisin did not differ from the controls. The concentrations of nisin estimated by competitive enzyme-linked immunosorbent assay (ELISA) were approximately 10-fold higher in the small intestine and 200-fold higher in feces than the corresponding concentrations estimated by a biological assay. This indicates that nisin was degraded or inactivated in the gastrointestinal tract, since fragments of this bacteriocin are detected by ELISA while an intact molecule is needed to retain biological activity.

Agar↗

Characterization of intestinal microbiota and response to dietary virginiamycin supplementation in the broiler chicken.

The inclusion of antibiotic growth promoters, such as virginiamycin, at subtherapeutic levels in poultry feeds has a positive effect on health and growth characteristics, possibly due to beneficial effects on the host gastrointestinal microbiota. To improve our understanding of the chicken gastrointestinal microbiota and the effect of virginiamycin on its composition, we characterized the bacteria found in five different gastrointestinal tract locations (duodenal loop, mid-jejunum, proximal ileum, ileocecal junction, and cecum) in 47-day-old chickens that were fed diets excluding or including virginiamycin throughout the production cycle. Ten libraries (five gastrointestinal tract locations from two groups of birds) of approximately 555-bp chaperonin 60 PCR products were prepared, and 10,932 cloned sequences were analyzed. A total of 370 distinct cpn60 sequences were identified, which ranged in frequency of recovery from 1 to 2,872. The small intestinal libraries were dominated by sequences from the Lactobacillales (90% of sequences), while the cecum libraries were more diverse and included members of the Clostridiales (68%), Lactobacillales (25%), and Bacteroidetes (6%). To assess the effects of virginiamycin on the gastrointestinal microbiota, 15 bacterial targets were enumerated using quantitative, real-time PCR. Virginiamycin was associated with increased abundance of many of the targets in the proximal gastrointestinal tract (duodenal loop to proximal ileum), with fewer targets affected in the distal regions (ileocecal junction and cecum). These findings provide improved profiling of the composition of the chicken intestinal microbiota and indicate that microbial responses to virginiamycin are most significant in the proximal small intestine.

Animals↗

The front line of enteric host defense against unwelcome intrusion of harmful microorganisms: mucins, antimicrobial peptides, and microbiota.

The intestinal tract is a complex ecosystem that combines resident microbiota and the cells of various phenotypes with complex metabolic activities that line the epithelial wall. The intestinal cells that make up the epithelium provide physical and chemical barriers that protect the host against the unwanted intrusion of microorganisms that hijack the cellular molecules and signaling pathways of the host and become pathogenic. Some of the organisms making up the intestinal microbiota also have microbicidal effects that contribute to the barrier against enteric pathogens. This review describes the two cell lineages present in the intestinal epithelium: the goblet cells and the Paneth cells, both of which play a pivotal role in the first line of enteric defense by producing mucus and antimicrobial peptides, respectively. We also analyze recent insights into the intestinal microbiota and the mechanisms by which some resident species act as a barrier to enteric pathogens. Moreover, this review examines whether the cells producing mucins or antimicrobial peptides and the resident microbiota act in partnership and whether they function individually and/or synergistically to provide the host with an effective front line of defense against harmful enteric pathogens.

Animals↗

Role of antibiotics and fungal microbiota in driving pulmonary allergic responses.

Over the past four decades, there has been a significant increase in allergy and asthma in westernized countries, which correlates with alterations in fecal microbiota (microflora) and widespread use of antibiotics (the "hygiene hypothesis"). Antibiotics also lead to overgrowth of the yeast Candida albicans, which can secrete potent prostaglandin-like immune response modulators. We have developed a mouse model of antibiotic-induced microbiota disruption that includes stable increases in gastrointestinal (GI) enteric bacteria and GI Candida levels with no introduction of microbes into the lungs. Mice are treated for 5 days with cefoperazone in the drinking water, followed by a single oral gavage of C. albicans. This results in alterations of GI bacterial populations and increased yeast numbers in the GI microbiota for at least 2 to 3 weeks and can drive the development of a CD4 T-cell-mediated allergic airway response to subsequent mold spore (Aspergillus fumigatus) exposure in immunocompetent mice without previous systemic antigen priming. The allergic response in the lungs is characterized by increased levels of eosinophils, mast cells, interleukin-5 (IL-5), IL-13, gamma interferon, immunoglobulin E, and mucus-secreting cells. In the absence of antibiotics, mice exposed to Aspergillus spores do not develop an allergic response in the airways. This study provides the first experimental evidence to support a role for antibiotics and fungal microbiota in promoting the development of allergic airway disease. In addition, these studies also highlight the concept that events in distal mucosal sites such as the GI tract can play an important role in regulating immune responses in the lungs.

Animals↗

Cultivable oral microbiota of domestic dogs.

Bacteria were isolated from the dental plaques of nine dogs and a sample of pooled saliva from five other dogs and were then identified by comparative 16S rRNA gene sequencing. Among 339 isolates, 84 different phylotypes belonging to 37 genera were identified. Approximately half of the phylotypes were identified to the species level, and 28% of these were considered members of the indigenous oral microbiota of humans. The 16S rRNA gene sequences of the remaining 44 phylotypes were not represented in GenBank, and most of these phylotypes were tentatively identified as candidate new species. The genera most frequently isolated from saliva were Actinomyces (26%), Streptococcus (18%), and Granulicatella (17%). The genera most frequently isolated from plaque were Porphyromonas (20%), Actinomyces (12%), and Neisseria (10%). A comparison of the DNA sequences from this study with sequences of the human microbiota available in GenBank showed that, on average, canine and human microbiotas differed by almost 7% in the 16S rRNA gene. In conclusion, this study has shown that the cultivable oral microbiotas of dogs and humans show significant differences.

Animals↗

Bacterial and fungal microbiota in relation to probiotic therapy (VSL#3) in pouchitis.

BACKGROUND: The intestinal microbiota plays a critical role in the pathophysiology of pouchitis, a major complication after ileal pouch anal anastomosis in patients with ulcerative colitis. Recently, controlled trials have demonstrated that probiotics are effective in maintenance of remission in pouchitis patients. However, the mechanism by which therapy with probiotics works remains elusive. This study explores the role of the bacterial and fungal flora in a controlled trial for maintenance of remission in pouchitis patients with the probiotic VSL#3 compound. METHODS: The mucosa associated pouch microbiota was investigated before and after therapy with VSL#3 by analysis of endoscopic biopsies using ribosomal DNA/RNA based community fingerprint analysis, clone libraries, real time polymerase chain reaction (PCR), and fluorescence in situ hybridisation. Patients were recruited from a placebo controlled remission maintenance trial with VSL#3. RESULTS: Patients who developed pouchitis while treated with placebo had low bacterial and high fungal diversity. Bacterial diversity was increased and fungal diversity was reduced in patients in remission maintained with VSL#3 (p = 0.001). Real time PCR experiments demonstrated that VSL#3 increased the total number of bacterial cells (p = 0.002) and modified the spectrum of bacteria towards anaerobic species. Taxa specific clone libraries for Lactobacilli and Bifidobacteria showed that the richness and spectrum of these bacteria were altered under probiotic therapy. CONCLUSIONS: Probiotic therapy with VSL#3 increases the total number of intestinal bacterial cells as well as the richness and diversity of the bacterial microbiota, especially the anaerobic flora. The diversity of the fungal flora is repressed. Restoration of the integrity of a "protective" intestinal mucosa related microbiota could therefore be a potential mechanism of probiotic bacteria in inflammatory barrier diseases of the lower gastrointestinal tract.

Adult↗

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.

Actinomyces↗

Gut microbiota dysbiosis and host metabolite-immune crosstalk drives the pathogenesis of neonatal lupus erythematosus: a multi-omics analysis.

BACKGROUND: Neonatal lupus erythematosus (NLE) is a rare autoimmune condition triggered by the transplacental transfer of maternal antibodies. Despite its recognized clinical manifestations, the underlying pathogenesis remains incompletely understood. This study seeks to explore the disruption of the gut microbiota-host metabolism-immune axis in anti-Ro/La-positive neonates, and to assess its potential role in the development of NLE. METHODS: This multicenter, cross-sectional study included 90 neonates, divided into three groups: 30 with neonatal lupus erythematosus (NLE), 30 with positive antibodies but without clinical manifestations (No-NLE), and 30 healthy controls. We performed 16 S rRNA sequencing to analyze gut microbiota composition, untargeted plasma metabolomic profiling, and proteomic analysis to identify alterations associated with the pathogenesis of NLE. RESULTS: We identified significant alterations in the gut microbiota, plasma metabolome, and proteome profiles of anti-Ro/La-positive neonates. NLE infants exhibited marked enrichment of Enterobacteriaceae and depletion of Bifidobacterium and Clostridium butyricum. Metabolomic analysis revealed hyperactivation of β-alanine and purine metabolism, along with impaired α-linolenic acid metabolism and endocannabinoid signaling. Proteomic profiling indicated aberrant protein expression that modulated IFN signaling, particularly within the C-type lectin receptor pathway. Dysregulation of the spleen tyrosine kinase (SYK) and high-affinity immunoglobulin epsilon receptor subunit gamma (FCER1G) decoupling was observed, correlating with elevated IFN-α and NF-κB p65 levels. Integrated correlation analysis revealed significant associations among differential microbial taxa, plasma metabolites, and proteins. Notably, E. coli-associated metabolites and proteins displayed inverse relationships with those associated with C. butyricum. CONCLUSIONS: These findings represent comprehensive evidence of dysregulation along the "gut microbiota-host metabolism-immune" axis in neonatal lupus erythematosus (NLE), providing novel insights into the disease's underlying heterogeneity.

Humans↗

The effect of clindamycin on the microbiota associated with refractory periodontitis.

The purpose of this investigation was to determine the effect of clindamycin hydrochloride, as an adjunct to scaling, on the microbiota associated with refractory periodontitis and to elucidate the probable causative bacteria associated with the disease. Microbial samples were collected from a subset of 9 patients with severe adult periodontitis who had not responded to conventional treatment modalities including the use of tetracycline and other antibiotics. Microbial samples were collected from a relatively deep site determined to be actively losing attachment and a comparably deep, but quiescent, control site in each patient prior to clindamycin therapy. Samples continued to be collected from the same sites for up to 1 year post-therapy. The microbial flora of each sample were enumerated by darkfield microscopy and predominant cultivable methods. Prior to clindamycin therapy, both active and control sites consisted on average of approximately 50% spirochetes and motile rods and 40% Gram-negative anaerobic rods. Bacteroides intermedius and Porphyromonas gingivalis (formerly B. gingivalis) were elevated in the active, as compared to control, sites and accounted for approximately 20% of the cultured microbiota in the former. Following treatment with clindamycin, the Gram-negative components of the microbiota were either eliminated or severely suppressed. At 1 year post-therapy, spirochetes and motile rods together accounted for about 15% of the microscopic flora. Total Gram-negative anaerobic rods accounted for approximately 20%, and B. intermedius and P. gingivalis combined accounted for less than 2% of the cultured microbiota from historical active sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Alveolar Bone Loss↗