Role of oral and gut microbiome in nitric oxide-mediated colon motility

Walker, Miriam Y.; Pratap, Siddharth; Southerland, Janet H.; Farmer-Dixon, Cherae; Kesavalu, Lakshmyya; Gangula, Pandu R.

doi:10.1016/j.niox.2017.06.003

Cited by 67 publications

(46 citation statements)

References 58 publications

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“…In the dependent form, three isoenzymes are present, the endothelial NO synthase [eNOS], neural NOS [nNOS], and iNOS. The latter is related to pro-inflammatory cytokines such as tumor necrosis factor α [TNF α], interleukin 1 (IL-1), and interferon γ (IFN-γ), so its overexpression must be regulated [94]. Increased NO synthesis by iNOS is a process that occurs during intestinal inflammation [95], which occurred in the experimental animals due to the presence of DSS.…”

Section: Discussionmentioning

confidence: 99%

Modification of In Vitro and In Vivo Antioxidant Activity by Consumption of Cooked Chickpea in a Colon Cancer Model

et al. 2020

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Chickpea has been classified as a nutraceutical food due to its phytochemical compounds, showing antioxidant, anti-inflammatory, and anticancer activity. To investigate this, we evaluated the effect of cooking on the nutritional and non-nutritional composition and the in vitro and in vivo antioxidant activity of chickpea seed. The latter was determined by the variation in the concentration of nitric oxide (NO), oxidized carbonyl groups (CO), malondialdehyde (MDA), and the expression of 4-hydroxy-2-nonenal (4-HNE) in the colon of male BALB/c mice fed with a standard diet with 10 and 20% cooked chickpea (CC). We induced colon cancer in mice by administering azoxymethane/dextran sulfate sodium (AOM/DSS); for the evaluation, these were sacrificed 1, 7, and 14 weeks after the induction. Results show that cooking does not significantly modify (p < 0.05) nutritional compounds; however, it decreases the concentration of non-nutritional ones and, consequently, in vitro antioxidant activity. The in vivo evaluation showed that animals administered with AOM/DSS presented higher concentrations of NO, CO, MDA, and 4-HNE than those in animals without AOM/DSS administration. However, in the three evaluated times, these markers were significantly reduced (p < 0.05) with CC consumption. The best effect on the oxidation markers was with the 20% CC diet, demonstrating the antioxidant potential of CC.

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Section: Discussionmentioning

confidence: 99%

Modification of In Vitro and In Vivo Antioxidant Activity by Consumption of Cooked Chickpea in a Colon Cancer Model

et al. 2020

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“…The polymicrobial nature of periodontal disease can promote chronic inflammation, not only in the oral cavity, but also in other places in the human body, such as the gut. Thus, the constituents of oral bacteria are directly related to the constituents of intestinal microbiota [ 27 , 28 ]. Studies suggest that innate immunity receptors, such as Toll-like receptors (TLRs), can detect a wide range of signals, like the microbe-associated molecular patterns (MAMPs), to regulate and maintain intestinal homeostasis.…”

Section: Discussionmentioning

confidence: 99%

Effects of β-Glucans Ingestion on Alveolar Bone Loss, Intestinal Morphology, Systemic Inflammatory Profile, and Pancreatic β-Cell Function in Rats with Periodontitis and Diabetes

et al. 2017

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This study aimed to evaluate the effects of β-glucan ingestion (Saccharomyces cerevisiae) on the plasmatic levels of tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10), alveolar bone loss, and pancreatic β-cell function (HOMA-BF) in diabetic rats with periodontal disease (PD). Besides, intestinal morphology was determined by the villus/crypt ratio. A total of 48 Wistar rats weighing 203 ± 18 g were used. Diabetes was induced by the intraperitoneal injection of streptozotocin (80 mg/kg) and periodontal inflammation, by ligature. The design was completely randomized in a factorial scheme 2 × 2 × 2 (diabetic or not, with or without periodontitis, and ingesting β-glucan or not). The animals received β-glucan by gavage for 28 days. Alveolar bone loss was determined by scanning electron microscopy (distance between the cementoenamel junction and alveolar bone crest) and histometric analysis (bone area between tooth roots). β-glucan reduced plasmatic levels of TNF-α in diabetic animals with PD and of IL-10 in animals with PD (p < 0.05). β-glucan reduced bone loss in animals with PD (p < 0.05). In diabetic animals, β-glucan improved β-cell function (p < 0.05). Diabetic animals had a higher villus/crypt ratio (p < 0.05). In conclusion, β-glucan ingestion reduced the systemic inflammatory profile, prevented alveolar bone loss, and improved β-cell function in diabetic animals with PD.

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“…Oral bacteria can directly or indirectly modulate the microbiome of the gall bladder and upper gastrointestinal tract, participating in the pathogenesis of GSD. Oral bacteria disrupt the synthesis of NO, the cofactor of eNOS, both in the vascular network and in the colon, and reduce the expression of the antioxidant protein Nrf2 and the bioavailability of NO, increasing the amount of reactive oxygen species [ 36 ].…”

Section: Oral Cavity Bacterial Communities and Gsdmentioning

confidence: 99%

Gallstone Disease and Microbiome

Григорьева

Romanova

2020

Microorganisms

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Gallstone disease (GSD) has, for many years, remained a high-cost, socially significant public health problem. Over the past decade, a number of studies have been carried out—both in humans and in animal models—confirming the role of the microbiota in various sections of the gastrointestinal tract as a new link in the etiopathogenesis of GSD. The microbiome of bile correlates with the bacterial composition of saliva, and the microbiome of the biliary tract has a high similarity with the microbiota of the duodenum. Pathogenic microflora of the oral cavity, through mechanisms of immunomodulation, can affect the motility of the gallbladder and the expression of mucin genes (MUC1, Muc3, MUC4), and represent one of the promoters of stone formation in the gallbladder. The presence of H. pylori infection contributes to the formation of gallstones and affects the occurrence of complications of GSD, including acute and chronic cholecystitis, cholangitis, pancreatitis. Intestinal bacteria (Clostridium, Bifidobacterium, Peptostreptococcus, Bacteroides, Eubacterium, and Escherichia coli) participating in the oxidation and epimerization of bile acids can disrupt enterohepatic circulation and lead to the formation of gallstones. At the same time, cholecystectomy due to GSD leads to the further transformation of the composition of the microbiota in various parts of the gastrointestinal tract, increasing the risk of developing stomach cancer and colorectal cancer. Further research is required to determine the possibility of using the evaluation of the composition of the microbiota of the gastrointestinal and biliary tracts as an early diagnostic marker of various gastroenterological diseases.

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Role of oral and gut microbiome in nitric oxide-mediated colon motility

Cited by 67 publications

References 58 publications

Modification of In Vitro and In Vivo Antioxidant Activity by Consumption of Cooked Chickpea in a Colon Cancer Model

Modification of In Vitro and In Vivo Antioxidant Activity by Consumption of Cooked Chickpea in a Colon Cancer Model

Effects of β-Glucans Ingestion on Alveolar Bone Loss, Intestinal Morphology, Systemic Inflammatory Profile, and Pancreatic β-Cell Function in Rats with Periodontitis and Diabetes

Gallstone Disease and Microbiome

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