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PubMed1991

Immunoadjuvant activity of oral Lactobacillus casei: influence of dose on the secretory immune response and protective capacity in intestinal infections.

Lactobacilli, often used as effectors of host functions, could play an important role in maintaining human health by controlling other intestinal microorganisms capable of producing harmful effects. Using an experimental model, we studied the effect of different oral doses of Lactobacillus casei on the secretory IgA response and the protective capacity of the microorganism in preventing intestinal infections. The optimization of the protective dose of Lb. casei by previous feeding and the use of the lactobacillus as an immunological way to control enteric infections were investigated. We found that conventional mice were protected against infection with Salmonella typhimurium and Escherichia coli by previous feeding for 2 consecutive days with a daily Lb. casei dose of 1.2 x 10(9) cfu/mouse. Previous feeding for 7 d proved less effective, and feeding for 5 d afforded no protection at all. We were also able to demonstrate that the protective effect of Lb. casei against Sal. typhimurium and Esch. coli was connected mainly with the high level of IgA antipathogen antibodies present in intestinal secretions. beta-Glucuronidase (EC 3.2.1.31) and beta-galactosidase (EC 3.2.1.23) activities, measured both in the intestinal fluid and histological samples, showed a marked increase in intestinal inflammatory response on day 5 of feeding. These results show that Lb. casei plays an important role in the prevention of enteric infections, a low dose being enough for protection against intestinal infections by increasing IgA secretion into the intestinal lumen, thus providing adequate defences for the mucosal surface. A previously administered dose of this magnitude could therefore be used as an oral adjuvant in preventing enteric infections.

Adjuvants, Immunologic↗
PubMed1981

Methyl mercury decomposition in mice treated with antibiotics.

The role of intestinal flora in the decomposition and faecal excretion of methyl mercury was studied in mice treated with antibiotics. The antibiotics, neomycin sulfate and chloramphenicol, were given to mice in drinking water for six days before intraperitoneal administration of methyl mercuric chloride (MMC), and intestinal microorganisms were thereby reduced. Inorganic and organic mercury were determined separately for faeces, intestinal contents and organs. On the fourth day after the mercury administration, the percentage ratios of inorganic mercury to total mercury in the contents of the caecum and large intestine were less in the mice treated with antibiotics, at 37% and 39%, respectively, than in the control mice (66% and 65%, respectively). Administration of the antibiotics reduced the excretion of inorganic mercury in the faeces to 26% of that of control mice and also reduced the excretion of total mercury to 60%. Reduction of intestinal microorganisms by the antibiotics was assumed to have caused the reduced decomposition of methyl mercury in the caecal contents and the reduced excretion of total mercury in the faeces.

Animals↗
PubMed1991

Decrease of gastrointestinal mucosal damage by salicyluric acid compared with salicylic acid in rabbits.

The gastrointestinal mucosal damage following the oral administration of salicylic acid or salicyluric acid was examined in rabbits using a scanning electron microscope. Six and 24 h after treatment with salicylic acid, morphological changes of gastric mucosa were recognized. In rabbits treated with salicyluric acid, however, severe damage in the gastric mucosa was not found after 24 h compared with the treatment with salicylic acid. Following the treatment with salicylic acid, some mucosal damage in the duodenum, jejunum and ileum was observed after 24 h. The surface character of the duodenal, jejunal, ileal, caecal and colonic mucosa were almost identical compared with the control following the treatment with salicyluric acid. It was reported that salicyluric acid is metabolized to salicylic acid by the intestinal microorganisms. From these results, it was suggested that prodrugs utilizing the metabolism of salicyluric acid to salicylic acid by intestinal microorganisms may be useful in reducing gastrointestinal mucosal damage.

Administration, Oral↗
PubMedDate not supplied

[Evaluation of a colorimetric method for studying the interaction between microorganisms and intestinal epithelial cells].

The aim of the present study was to gain further insight on the reliability of the colorimetric determination of the activity of bacterial nitrate reductase to evaluate bacterial concentrations and interaction between microorganisms and enterocyte-like cells. Nitrite produced after incubation of the samples with a nitrate-formate solution was determined with a diazotization reaction with sulphanilic acid and N-naphthyl-ethylene-diamonium dichloride. Cell association assays were performed with differentiated Caco-2 cells. A biphasic relationship was found between nitrite concentration and bacterial densities. This behavior seems to be due to the sigmoideal character of the kinetics of nitrate reduction. Association to Caco-2 cells was strongly strain dependent being Staphylococcus aureus ATCC 25923 the strain showing the highest values of association. For some strains, percentages of association calculated on the basis of the colorimetric assay were significantly higher than those calculated in terms of viable counts. Bacterial association with enterocyte-like cells can be evaluated by measures of the activity of bacterial nitrate reductase provided that the biphasic relationship between bacterial and nitrite concentrations is taken into account for the calculations. Results presented in this paper show the applicability of the colorimetric method to assess the amount of microorganisms associated to human enterocytes in culture.

Bacillus cereus↗
PubMed1999

Advanced analysis of biotin metabolites in body fluids allows a more accurate measurement of biotin bioavailability and metabolism in humans.

In previous studies, the bioavailability of biotin in humans was estimated from the recovery of biotin in urine; urinary biotin was measured by microbial growth assays or assays of avidin-binding activity. These assays underestimate concentrations of biotin metabolites, which originate from beta-oxidation, sulfur oxidation or a combination. We have developed an HPLC/avidin-binding assay that is specific for biotin and its metabolites. With the use of the HPLC/avidin-binding assay, TLC and derivatization with p-dimethylaminocinnamaldehyde, we have identified and quantitated biotin and metabolites in urine from six healthy adults. Of that total, biotin accounted for 32+/-12%, bisnorbiotin for 52+/-15%, bisnorbiotin methyl ketone for 7.9+/-5.8%, biotin-d,l-sulfoxide for 4.0+/-3.2% and biotin sulfone for 3.6+/-1.9%. After intravenous administration of 18.4 micromol of biotin, the urinary excretion of biotin metabolites increased 21-130 times above baseline values. Because the biliary excretion of biotin is quantitatively minor (1.9+/-0.2% of an intravenous [14C]biotin dose in rats), intravenously administered biotin is not exposed to intestinal microorganisms. Thus we conclude that biotin metabolites in human urine originate from biotin catabolism in human tissues rather than biotin catabolism by intestinal microorganisms. With the use of the HPLC/avidin-binding assay, we estimated the bioavailability of biotin in adults from the urinary excretion of biotin and metabolites after ingestion of 2.1, 8.2 and 81.9 micromol of biotin. These data provide evidence that biotin is nearly completely absorbed.

Animals↗
PubMed1982

Origin of excess urinary nitrate in the rat.

The ability of intestinal microorganisms to N-oxidize nitrogenous compounds to nitrite or nitrate was evaluated both in vivo and in vitro. Nitrate balance studies with germ-free and conventional rats indicated that the host and not the microbial flora is responsible for excess urinary nitrate. In vitro studies showed that most intestinal microorganisms are not able to N-oxidize nitrogenous compounds to nitrite. Although the metabolic pathway for endogenous nitrate formation remains unknown, the capacity of the rats to N-oxidize acetohydroxamate and hydroxylamine to nitrate indicates that such compounds could be intermediates in nitrate synthesis.

Amino Acids↗
PubMed1999

Where does indolylacrylic acid come from?

In addition to the main catabolic routes of tryptophan (Trp), there exist minor and less thoroughly investigated pathways; one of these leads to indolylacrylic acid (IAcrA). IAcrA is a plant growth hormone, whereas its biological role in animals is still obscure, as is the way and site where it is formed in the organism. A two-stage production is likely: Intestinal microorganisms catabolize Trp to indole derivatives which are then absorbed and converted to IAcrA and its glycine conjugate, indolylacryloylglycine (IAcrGly). Our finding of IAcrGly in the urine of proven germ-free piglets points to the possibility that Trp can be converted to IAcrA without the intervention of intestinal microorganisms. Seasonal and age variations, influence of light and connection with photodermatoses have been reported. Besides other pathological conditions the differences in IAcrGly excretion relative to normal controls were especially pronounced in some myopathies, namely in boys with Duchenne muscular dystrophy.

Aging↗
PubMed1978

Effect of orally administered duodenal fluid on serum proteins in neonatal calves.

This study was to determine if orally administered duodenal fluid, as a source of intestinal microorganisms, would influence absorption of gamma-globulin of colostrum in newborn calves. Duodenal fluid was obtained 2 h postfeeding from a cannulated milk-fed calf. Twenty-seven male and female Holstein calves obtained within 6 h of birth were assigned randomly to one of three treatments: 1) colostrum alone, 2) 200 ml duodenal fluid immediately followed by colostrum, and 3) 200 ml duodenal fluid followed 3 h later by colostrum. Pooled colostrum was fed at 10% of body weight in two daily feedings. Total protein, albumin, alpha-globulin, beta-globulin, and gamma-globulin of blood serum were determined prior to colostrum consumption, and again 24 and 48 h after administration of duodenal fluid. Total proteins, beta-globulin, and gamma-globulin of serum increased with age in all calves. Inocula interference with absorption was indicated by depressed values of serum in calves of treatment 3 as compared to treatment 1 calves for protein (5.28 to 6.28 g/dl), beta-globulin (.67 to .87 g/dl), and gamma-globulin (.76 to 1.33 g/dl). Protein was also lower in calves of treatment 3 (6.05 g/dl) compared to uninoculated calves (6.28 g/dl). Malabsorption of colostral proteins may be related to early establishment of large numbers of intestinal microorganisms in the newborn calf.

Animals↗
PubMed1979

Methylmalonic acid metabolism of germfree and conventional vitamin B-12 deprived rats fed precursors of methylmalonate.

Experiments using germfree (GF), ex-germfree (XGF) and conventional (CONV) rats were conducted to study the relationship of intestinal microorganisms to vitamin B-12 (B-12) status and to methylmalonic acid (MMA) excretion of the host animal, since B-12 depleted GF rats have been found to excrete less than expected level of urinary MMA. The possibility that the GF rat lacks sufficient precursor of MMA was tested by feeding GF, XGF and CONY rats diets low or high in MMA precursors and examining urinary excretion of MMA and formiminoglutamic acid at intervals. The possibility that the GF rat may metabolize propionate and MMA differently from the CONV rat was examined by a MMA loading-recovery study and a CO2 collection study after [14C]propionate injection. Plasma and tissue B-12 levels were determined at the beginning and the end of the study. Results indicate that 1) lack of sufficient precursor of MMA is partly responsible for the failure of GF, B-12 deficient rat to excrete MMA, 2) GF and CONV rats metabolize propionate and MMA by the same pathways and 3) the presence of intestinal microorganism depletes the body B-12 store of the rat.

Animals↗
PubMedDate not supplied

[Interrelationship between the intestinal microflora of lackey moth, brown-tail moth and the entomopathogenic bacterium Bacillus thuringiensis].

The interrelationship between the intestine microflora of lackey moth (Malacosoma neustria L.), brown-tail moth (Nygmia phaeorrhoea L.) and entomopathogenic bacteria Bacillus thuringiensis (Berl.), Bac. thuringiensis var. galleriea, and Bac. thuringiensis KR3 was studied in vitro. Various organisms of the intestine microflora of lackey moth display bacteriostatic action towards Bac. thuringiensis var. galleriea and Bac. thuringiensis KR3 which is not typical of the microflora of brown-tail moth that manifests mainly the batericidal action. Yeast cultures have been isolated from the intestines of lackey moth; the cultures stimulated growth of the studied entomopathogenic bacterial test cultures. Therefore, weak virulent action of Bac. thuringiensis towards brown-tail moth, as compared to its action on lackey moth, may be due to the bactericidal properties of some intestine microorganisms of brown-tail moth, and also the absence in their intestines of microorganisms stimulating growth of the entomopathogenic bacteria.

Animals↗
PubMed2004

Microflora in inflammatory bowel diseases: a pediatric perspective.

Several lines of evidence link inflammatory bowel diseases to modifications of intestinal microflora. Epidemiologic and clinical data suggest a triggering role for select agents in ulcerative colitis and in Crohn disease. Experimental evidence indicates that intestinal microorganisms are needed for developing intestinal inflammation in IL-10 knockout mice, and this is associated with an increased number of adherent clostridia and a decrease of lactobacilli and bifidobacteria. It may be hypothesized that a host-agent-specific relationship leads to an abnormal immune response, which may be genetically driven in select inflammatory bowel diseases. However, different from adults, the pattern of intestinal microflora undergoes profound changes during the early stage of life, contributing to the development of the immune system. A close relationship exists between microbiologic and immunologic imprinting. The microbiologic imprinting in neonates may be modified using bacterial probiotics that colonize the intestine, modify the immune response, and decrease the risk for atopy. Probiotics may decrease the recurrences of inflammatory bowel diseases. Preliminary evidence of intestinal antiinflammatory effects has been detected in children with cystic fibrosis. Overall these data provide the rationale to investigate the interaction between intestinal microflora and the local and general immune response in children with, or at risk for, inflammatory bowel diseases. This approach may be a key for understanding the pathophysiology of intestinal inflammation and may disclose novel strategies to educate better the immune system, particularly during its developmental stage.

Animals↗
PubMed1990

Isolation and structural elucidation of biotransformation products from acarbose.

Following oral administration the a-glucosidase inhibitor acarbose (O-4,6-dideoxy-4-[[(1S,4R,5S,6S)-4,5,6-trihydroxy-3-(hydroxymethyl) -2-cyclohexen-1-yl]amino]-a-D-glucopyranosyl-(1----4)-O-a-D-glu copyranosyl-(1----4)-D-glucopyranose, Bay g 5421) is degraded by digestive enzymes and/or intestinal microorganism. The effect of anaerobic intestinal bacteria can be studied in an in vitro model which involves the incubation of acarbose with human or animal intestinal flora. Acarbose and nine biotransformation products can be isolated from the incubation mixture. These products were identified by nuclear magnetic resonance and mass spectrometry as so-called component 2 (loss of the terminal glucose), component 1 (loss of both glucose rings), hexose homologues of acarbose and component 2, methyl homologues of acarbose, butyric acid ester of component 2, basic disaccharide (loss of the cyclitol ring of component 2), delta-aminovaleric acid and gamma-aminobutyric acid. Following oral administration of [14C]-acarbose to healthy volunteers, 35% of the radioactivity was excreted in the form of at least 13 metabolites in the urine. Three of the metabolites were isolated by Craig countercurrent distribution and ion-pair HPLC and characterized by virtue of their nuclear magnetic resonance and mass spectra as derivatives of 4-methylpyrogallol. Two were shown to be monomethylether-monosulphates while the third was a monosulphate-monoglucuronide. The synthesis of ten reference substances and the comparison of HPLC and UV data clearly indicated that the majority of the non-isolated metabolites were also 4-methylpyrogallol derivatives. The peculiarities of the nuclear magnetic resonance and mass spectra of this type of compound are discussed.

Acarbose↗
PubMed2026

Intestinal content accelerates muscle protein degradation in red shrimp (Solenocera crassicornis) during refrigeration: Insights from metagenomics and metabolomics.

This study systematically explored the effects of intestinal components on muscle quality deterioration and protein degradation of red shrimp during refrigerated storage. The results demonstrated that refrigeration induced continuous quality degradation and muscle protein breakdown in red shrimp, whereas eliminating intestinal tissues effectively retarded muscle spoilage and protein degradation, and optimized muscle texture. The intestinal microorganisms could secrete extracellular proteases to promote muscle protein degradation were primarily Vibrio, Bacillus, Pseudomonas, Photobacterium, and Shewanella. These microorganisms promote protein degradation by secreting zinc proteases, serine proteases, and aspartyl proteases. This study elucidates the molecular mechanisms of intestinal microbial metabolism influences the muscle protein degradation of red shrimp during refrigeration. The findings provide a theoretical foundation for precise regulation of intestinal-targeted microorganisms, thereby maintaining optimal quality of shrimps during refrigeration.

Animals↗
PubMed2004

Reduced ratio of protective versus proinflammatory cytokine responses to commensal bacteria in HLA-B27 transgenic rats.

Germ-free HLA-B27 transgenic (TG) rats do not develop colitis, but colonization with specific pathogen-free (SPF) bacteria induces colitis accompanied by immune activation. To study host-dependent immune responses to commensal caecal bacteria we investigated cytokine profiles in mesenteric lymph node (MLN) cells from HLA-B27 TG versus nontransgenic (non-TG) littermates after in vitro stimulation with caecal bacterial lysates (CBL). Supernatants from CBL-stimulated unseparated T- or B- cell-depleted MLN cells from HLA-B27 TG and non-TG littermates were analysed for IFN-gamma, IL-12, TNF, IL-10 and TGF-beta production. Our results show that unfractionated TG MLN cells stimulated with CBL produced more IFN-gamma, IL-12 and TNF than did non-TG MLN cells. In contrast, CBL-stimulated non-TG MLN cells produced more IL-10 and TGF-beta. T cell depletion abolished IFN-gamma and decreased IL-12 production, but did not affect IL-10 and TGF-beta production. Conversely, neither IL-10 nor TGF-beta was produced in cultures of B cell-depleted MLN. In addition, CD4(+) T cells enriched from MLN of HLA-B27 TG but not from non-TG rats produced IFN-gamma when cocultured with CBL-pulsed antigen presenting cells from non-TG rats. Interestingly, IL-10 and TGF-beta, but not IFN-gamma, IL-12 and TNF were produced by MLN cells from germ-free TG rats. These results indicate that the colitis that develops in SPF HLA-B27 TG rats is accompanied by activation of IFN-gamma-producing CD4(+) T cells that respond to commensal bacteria. However, B cell cytokine production in response to components of commensal intestinal microorganisms occurs in the absence of intestinal inflammation.

Animals↗
PubMed1966

Growth and invasiveness of Candida albicans in the germ-free and conventional mouse after oral challenge.

Candida albicans was established in large numbers throughout the gut after one oral challenge in the germ-free and in the conventional mouse. Of the strains tested, only the germ-free ND 1 mouse appeared to be susceptible to infection, and this was confined to the stomach mucosa; lesions contained large numbers of hyphal and mycelial forms with blastospores. These forms were also seen in the gut of resistant germ-free ND 4 mice after challenge. Only budding yeast forms were seen in the gut contents from conventional animals. The concentration of sulfhydryl-containing compounds was decreased in the stomach contents from germ-free mice. The stomach tissue of conventional animals seemed to be more acidic than that of germ-free animals, and association of C. albicans with conventional mice neutralized some of this acidity. E(h) values of contents from the gut of unchallenged mice were usually higher in conventional than in germ-free animals; after challenge, the E(h) in both groups decreased. Some reciprocal effects of intestinal microorganisms and host are discussed in relation to intestinal candidiasis.

Animals↗