scholarly journals Assessment of intermediate and long chains agave fructan fermentation on the growth of intestinal bacteria cultured in a gastrointestinal tract simulator

2019 ◽  
Vol 19 (2) ◽  
pp. 827-838 ◽  
Author(s):  
R. García-Gamboa ◽  
◽  
M. S. Gradilla-Hernández ◽  
R. I. Ortiz-Basurto ◽  
R. A. García-Reyes ◽  
...  
2010 ◽  
Vol 43 (4) ◽  
pp. 393-395 ◽  
Author(s):  
Kleber Giovanni Luz ◽  
Felipe Francisco Tuon ◽  
Maria Irma Seixas Duarte ◽  
Guilherme Mariz Maia ◽  
Paulo Matos ◽  
...  

INTRODUCTION: Visceral leishmaniasis (VL) is a neglected tropical disease with a complex immune response in different organs. This pattern of organ-specific immune response has never been evaluated in the gastrointestinal tract. The aim of this study was to determine the in situ immune response in duodenal biopsies on patients with VL. METHODS: A case-control study was conducted on 13 patients with VL in comparison with nine controls. The immune response was evaluated using immunohistochemistry, for CD4, CD8, CD68, IL-4, IFN-γ, TNF-α and IL-10. Histological findings from the villi, crypts and inflammatory process were analyzed. RESULTS: All the cases of VL presented Leishmania antigens. No antigen was detected in the control group. The villus size was greater in the VL patients (p < 0.05). CD68 (macrophages) and CD4 levels were higher in the VL patients (p < 0.05). No differences in the expression of CD8, TNF-α, IL-10 or IL-4 were demonstrated. The number of cells expressing IFN-γ was lower in the VL patients (p < 0.05). CONCLUSIONS: Low levels of cytokines were found in the gastrointestinal tract of patients with VL. This pattern was not found in other organs affected by the disease. Immunotolerance of this tissue against Leishmania could explain these findings, as occurs with intestinal bacteria.


2012 ◽  
Vol 17 (7) ◽  
pp. 957-965 ◽  
Author(s):  
Syed Ahmad ◽  
Mark A. Hughes ◽  
Li-An Yeh ◽  
John E. Scott

The active metabolite of the chemotherapeutic irinotecan, SN-38, is detoxified through glucuronidation and then excreted into the gastrointestinal tract. Intestinal bacteria convert the glucuronidated metabolite back to the toxic SN-38 using β-glucuronidase (GUS), resulting in debilitating diarrhea. Inhibiting GUS activity may relieve this side effect of irinotecan. In this study, we sought to determine whether any known drugs have GUS inhibitory activity. We screened a library of Food and Drug Administration–approved drugs with a cell-free biochemical enzyme assay using purified bacterial GUS. After triage, five drugs were confirmed to inhibit purified bacterial GUS. Three of these were the monoamine oxidase inhibitors nialamide, isocarboxazid, and phenelzine with average IC50 values for inhibiting GUS of 71, 128, and 2300 nM, respectively. The tricyclic antidepressant amoxapine (IC50 = 388 nM) and the antimalarial mefloquine (IC50 = 1.2 µM) also had activity. Nialamide, isocarboxazid, and amoxapine had no significant activity against purified mammalian GUS but showed potent activity for inhibiting endogenous GUS activity in a cell-based assay using living intact Escherichia coli with average IC50 values of 17, 336, and 119 nM, respectively. Thus, nialamide, isocarboxazid, and amoxapine have potential to be repurposed as therapeutics to reduce diarrhea associated with irinotecan chemotherapy and warrant further investigation for this use.


1993 ◽  
Vol 39 (9) ◽  
pp. 841-845 ◽  
Author(s):  
Xue Bin Zhang ◽  
Yoshiyuki Ohta

The extent to which lactic acid bacteria, intestinal bacteria, and yeast from the gastrointestinal tract of rats suppress the absorption of 3-amino-1,4-dimethyl-5H-pyrido(4,3-b)indole (Trp-P-1) was investigated. Trp-P-1 was absorbed from the small intestine very rapidly, but in the stomach it was slowly absorbed, requiring 1 or 2 h after administration. When mixtures of Trp-P-1 and freeze-dried microorganisms were administered to rats for 1 h, the amounts of Trp-P-1 absorbed from the small intestine were significantly reduced, and the levels of Trp-P-1 in blood decreased by 40.4–64.7% compared with a control in which only Trp-P-1 was administered. There were no significant differences between the organisms used. In vitro, freeze-dried cells of the strains tested bound 51-97% of Trp-P-1. The Trp-P-1 bound to cells was effectively extracted by aqueous methanol, ethanol, ammonia (50 g/L), and solutions of MgCl2 and CaCl2 (100 mM/mL), but little was extracted by water and solutions of KCl, NaCl, and buffers at various pH values.Key words: Trp-P-1, gastrointestinal absorption, binding, intestinal bacteria, mutagen–carcinogen.


1969 ◽  
Vol 20 (4) ◽  
pp. 725 ◽  
Author(s):  
AC Bray

In a series of experiments with sheep maintained on high sulphur rations, measurements were made on the levels of 35S in urine, faeces, and various body fluids following single intravenous infusions of sodium [3%]sulphate and single infusions of sodium [35S]sulphate or sodium [353]sulphide into the gastrointestinal tract. Sulphide was rapidly absorbed from the duodenum and post-duodenal intestinal tract, an estimated 40–90% of the dose being absorbed within 60 min. Absorption of sulphate from the same region was much slower, 25% or less being absorbed over a 60-min interval. An attempt to use antibiotics to eliminate the effects of the intestinal bacteria on the metabolism of [35S]sulphate before absorption was not conclusive. Following intravenous administration of sodium [35S]sulphate, 12–19% of the dose was recovered in the faeces within 6 days. This activity appeared to be due to secretion into the post-ruminal tract rather than to return of 35S by salivary secretion or by passage across the rumen wall. Sodium [35S]sulphate was reduced to sulphide in the rumen and appreciable amounts appeared to be absorbed from this organ. The variations in total sulphur and sulphide of rumen digesta, urinary total sulphur, and blood inorganic sulphate levels during the day appeared to be related. Whole blood inorganic sulphate sulphur levels varied between 2 and 6 mg%. Urinary excretion following intravenous administration of 35S was extremely rapid, at least 70% of the dose being collected within 24 hr.


2021 ◽  
Author(s):  
Alba Tamargo ◽  
Natalia Molinero ◽  
Julián J. Reinosa ◽  
Victor Alcolea-Rodríguez ◽  
Raquel Portela ◽  
...  

Abstract Microplastics are a widely recognized global problem due to their prevalence in natural environments and the food chain. However, the impacts of microplastics on human microbiota and their possible biotransformations during the gastrointestinal tract have not been well reported. To evaluate the potential risks of microplastics at the digestive level, completely passing a single dose of polyethylene terephthalate (PET) through the gastrointestinal tract was simulated by combining a harmonised static model and the dynamic gastrointestinal simgi® model, which recreates the different regions of the digestive tract in physiological conditions. PET MPs started several biotransformations in the gastrointestinal tract and appeared to expose the colon in ways that were structurally different from the original forms. We report that the feeding with microplastics alters human microbial colonic community composition, and hypothesize that some members of the colonic microbiota could adhere to MPs surface promoting the formation of biofilms. The work presented here indicates that microplastics are indeed capable of digestive-level health effects. Considering this evidence and the increasing exposure to microplastics in consumer foods and beverages, the impact of plastics on the functionality of the gut microbiome and their potential biodegradation through digestion and intestinal bacteria merits critical investigation.


2000 ◽  
Author(s):  
Γεώργιος Κούκης

Η μικροβιακή διαμετάθεση αποτελεί πιθανώς την αιτία της λοίμωξης από εντερικής προέλευσης μικροοργανισμούς .οι Danner και συν(1988) βρήκαν μικροβιαιμία από εντερικής προέλευσης μικροοργανισμούς στο 54% των ασθενών μιας ΜΕΘ με τοξιναιμία και στο 24% χωρίς τοξιναιμία. Οι Fiddian-Green και Gnantz (1987) ενοχοποιούν την διαμετάθεση ως αιτία των λοιμώξεων από εντερικής προέλευσης μικροοργανισμούς στο 54%σε ασθενείς που υφίστανται χειρουργικές επεμβάσεις επί της κοιλιακής αορτής δεδομένου ότι η επίπτωση των λοιμώξεων αυτών αυξάνεται αλματωδώς όσο αυξάνεται η οξέωση του παχέος εντέρου ενδοβλεννογονίως. Η ενδοβλεννογόνιος οξέωση προηγείται κατά μερικές ημέρες των ενδοσκοπικών ευρημάτων της ισχαιμικής κολίτιδας η οποία έπεται κατά δυο ως δεκατέσσερις ημέρες της εμφάνισης μικροοργανισμών στο αίμα. Επίσης οι Fabian και συν(1988) απομόνωσαν εντερικής προέλευσης μικροοργανισμούς στο αίμα ασθενών της Μ.Ε.Θ, στην συντριπτική πλειοψηφία των οποίων συνοδευόταν από αύξηση των επίπεδων του γαλακτικού οξέος, που ερμηνεύτηκε ως ένδειξη ιστικής ισχαιμίας. (Antonsson και Fiddian-Green 1991).Από την παρούσα εργασία προκύπτουν αρκετά συμπεράσματα με πρώτο και κύριο την στατιστική απόδειξη της μειώσεως των λοιμώξεων όταν έχουμε μείωση του μικροβιακού φορτίου του εντέρου. Την μείωση αυτή την επιτύχαμε με τον μηχανικό καθαρισμό του εντέρου, μια διαδικασία εύκολη, χαμηλού κόστους και άριστα ανεκτή από τον ασθενή.ΕΝΔΕΙΚΤΙΚΗ ΒΙΒΛΙΟΓΡΑΦΙΑ1. Antonsson J.B. and Fiddian Green R.G. The role of the gut in shock and multiple system organ failure. Eur. J.Syrg. 157: 3, 19912. Berg R.D. Bacterial translocation from the gastrointestinal tract of mice receiving immunosuppressive agents. Current Microbiol. 8: 285, 1983 (ως Berg R.D. 1983).3. Cuevas P and Fine J. Route of absorption from the intestine in the non septic shock. J. Reticuloedothel. Soc 11: 535, 1972 (ως Cuevas και Fine 1972-β).4. Deitch E.A. Bacterial translocation from the gut. A mechanism of infection. J Burn Care Rehabit. 8- 475, 1987 (ως Deitch E.A 1987).5. Fiddian-Green R.G. Splachnic ischemia and multiple organ failure in the critically ill. Ann. Coll. Surg. Engl. 70: 128, 1988 (ως Fiddian Green R.G. 1988).6. Gans H. and Matsumoto K. The escape of endotoxine from the intestine S.G.O. 139:395, 1974.7. Haglund U, Abe T, Cren C, Braide L and Lundgreen O. The intestinal mucosal lesions in shock. Eur. Surg. Res. 8: 435,1976 (ως Hanglud και συν. 1976).8. Levin J.Tomasulo P.A. and Oser R.S. Detection of endotoxine in human blood and demonstration of an inhibitor. J. Lab. Clin. Med. 75: 903, 1070.9. Owens W.E. and Berg R.D. Bacterial translocation coli from the gastrointestinal tract of athymic (nu/nu) mice. Infect. Immun. 27: 461, 1980.10. Wells C.L, Maddaus M.A, Hechoreck R.P, Simmons R.I. Role of macrophage in tranlocation of intestinal bacteria. Arch. Surg


2020 ◽  
Author(s):  
Vincent Saillant ◽  
Damien Lipuma ◽  
Emeline Ostyn ◽  
Laetitia Joubert ◽  
Alain Boussac ◽  
...  

AbstractEnterococcus faecalis is a commensal Gram-positive pathogen found in the intestines of mammals, and is also a leading cause of severe infections occurring mainly among antibiotic-treated dysbiotic hospitalized patients. Like most intestinal bacteria, E. faecalis does not synthesize heme. Nevertheless, environmental heme can improve E. faecalis fitness by activating respiration metabolism and a catalase that limits hydrogen peroxide stress. Since free heme also generates redox toxicity, its intracellular levels need to be strictly controlled. Here, we describe a unique transcriptional regulator, FhtR, (Faecalis heme transport Regulator), which manages heme homeostasis by controlling an HrtBA-like efflux pump (named HrtBAEf). We show that FhtR, by managing intracellular heme concentration, regulates the functional expression of the heme dependent catalase A (KatA), thus participating in heme detoxification. The biochemical features of FhtR binding to DNA, and its interactions with heme that induce efflux, are characterized. The FhtR-HrtBAEf system is shown to be relevant in a mouse intestinal model. We further show that FhtR senses heme from blood and hemoglobin but also from crossfeeding by Escherichia coli. These findings bring to light the central role of FhtR heme sensing in response to heme fluctuations within the gastrointestinal tract, which allow this pathogen to limit heme toxicity while ensuring expression of an oxidative defense system.ImportanceEnterococcus faecalis, a normal, harmless colonizer of the human intestinal flora can cause severe infectious diseases in immunocompromised patients, particularly those that have been heavily treated with antibiotics. Therefore, it is important to understand the factors that promote its resistance and its virulence. Here, we report a new mechanism used by E. faecalis to detect the concentration of heme, an essential but toxic metabolite that is present in the intestine. E. faecalis needs to scavenge this molecule to respire and fight stress generated by oxydants. Heme sensing triggers the synthesis of a heme efflux pump that balances the amount of heme inside the bacteria. With this mechanism, E. faecalis can use heme without suffering from its toxicity.


2008 ◽  
Vol 53 (No. 4) ◽  
pp. 184-192 ◽  
Author(s):  
U. Schoenhusen ◽  
J. Voigt ◽  
U. Hennig ◽  
S. Kuhla ◽  
R. Zitnan ◽  
...  

D-alanine (DAL) has been successfully used as a marker of bacterial nitrogen (N) in the small intestine of cows. This study compares DAL contents of intestinal bacteria in digesta of cows and pigs with respect to diet and sampling site. In isolated ileal bacteria of pigs a DAL/N ratio (41.72 ± 3.19 mg/g, <I>n</I> = 18) was found, which was not different from that in rumen bacteria (40.11 ± 1.95 mg/g, <I>n</I> = 18) but higher than in duodenal bacteria of cows (38.09 ± 2.09 mg/g, <I>n</I> = 18, <I>P</I> < 0.001). The DAL/N ratio in ileal bacteria of pigs was independent of the diet (<I>P</I> = 0.38) but it tended to be affected by the animal (<I>P</I> = 0.095). In bacterial preparations derived from cows, the DAL/N ratio depended on the diet (<I>P</I> = 0.04) and the site of sampling (<I>P</I> = 0.004). Our findings indicate that a general value for DAL/N ratio in pig or cow intestinal contents to calculate bacterial N should not be used.


2017 ◽  
Vol 26 (4) ◽  
pp. 368-376 ◽  
Author(s):  
Kosuke Mima ◽  
Shuji Ogino ◽  
Shigeki Nakagawa ◽  
Hiroshi Sawayama ◽  
Koichi Kinoshita ◽  
...  

2019 ◽  
Vol 5 (1) ◽  
pp. 33-39
Author(s):  
Kathleen Morrisroe ◽  
Murray Baron ◽  
Tracy Frech ◽  
Mandana Nikpour

Systemic sclerosis is a multi-organ autoimmune disease characterized by vasculopathy and fibrosis, and it is arguably the most devastating of the rheumatological diseases. The gastrointestinal tract is the most commonly involved internal organ in systemic sclerosis. Gastrointestinal tract involvement is reported in up to 90% of SSc patients, is the leading cause of morbidity, and is the third most common cause of mortality in this disease. Among all gastrointestinal tract manifestations, small intestinal bacterial overgrowth is one manifestation that may be ameliorated and even eradicated with appropriate treatment, if recognized early. Small intestinal bacterial overgrowth occurs with a prevalence of approximately 39% in systemic sclerosis and presents with a range of non-specific gastrointestinal tract symptoms, including diarrhea, flatulence, abdominal pain, bloating, and early satiety. These manifestations occur due to an alteration and overgrowth of small intestinal bacteria occurring in the setting of gastrointestinal tract dysmotility and slow transit time. The clinical diagnosis of small intestinal bacterial overgrowth is commonly based on the presence of characteristic clinical symptoms together with a positive hydrogen breath test and response to a therapeutic trial of oral antibiotics used sequentially. Almost two-thirds of systemic sclerosis patients with small intestinal bacterial overgrowth have an improvement in their gastrointestinal tract symptoms with rotating antibiotics. Untreated small intestinal bacterial overgrowth can lead to malnutrition, and thus an important aspect of treatment is the identification and treatment of any associated vitamin and mineral deficiencies. This article focuses on small intestinal bacterial overgrowth, an important and understudied area in systemic sclerosis that remains a diagnostic and therapeutic challenge for both patients and clinicians alike.


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