Relevant bibliographies by topics / Digestive inflammation

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Digestive inflammation'

Author: Grafiati
Published: 25 January 2025

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Journal articles on the topic "Digestive inflammation"

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Waldum, Helge, and Reidar Fossmark. "Inflammation and Digestive Cancer." International Journal of Molecular Sciences 24, no. 17 (August 31, 2023): 13503. http://dx.doi.org/10.3390/ijms241713503.

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Chronic inflammation is linked to carcinogenesis, particularly in the digestive organs, i.e., the stomach, colon, and liver. The mechanism of this effect has, however, only partly been focused on. In this review, we focus on different forms of chronic hepatitis, chronic inflammatory bowel disease, and chronic gastritis, conditions predisposing individuals to the development of malignancy. Chronic inflammation may cause malignancy because (1) the cause of the chronic inflammation is itself genotoxic, (2) substances released from the inflammatory cells may be genotoxic, (3) the cell death induced by the inflammation induces a compensatory increase in proliferation with an inherent risk of mutation, (4) changes in cell composition due to inflammation may modify function, resulting in hormonal disturbances affecting cellular proliferation. The present review focuses on chronic gastritis (Helicobacter pylori or autoimmune type) since all four mechanisms may be relevant to this condition. Genotoxicity due to the hepatitis B virus is an important factor in hepatocellular cancer and viral infection can similarly be central in the etiology and malignancy of inflammatory bowel diseases. Helicobacter pylori (H. pylori) is the dominating cause of chronic gastritis and has not been shown to be genotoxic, so its carcinogenic effect is most probably due to the induction of atrophic oxyntic gastritis leading to hypergastrinemia.
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Sumantran, Venil N., and Girish Tillu. "Cancer, Inflammation, and Insights from Ayurveda." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/306346.

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A recent, exciting discovery relates to the concept of “shared pathology” between cancer and metabolic syndrome. One major pathway common to cancer and metabolic syndrome is chronic inflammation, which is a major driving force in carcinogenesis. Indeed, chronic inflammation precedes most cancers and is considered a “hallmark” of the neoplastic process. We discuss molecular and biochemical evidence which links diet, obesity, abnormal lipid metabolism, and type 2 diabetes mellitus with chronic inflammation. We also explain how each of these factors is linked with biochemical aberrations of carcinogenesis and the prevalence and risk of cancer. While there are reliable biomarkers for chronic inflammation, there are few markers for a mechanistic link between early inflammation and digestive disorders. Discovery of such a marker could lead to identification of a new subtype of patients with digestive disorders that predispose them to cancer and/or metabolic syndrome. In this context, we discuss the ayurvedic concept of “Ama” which is thought to be a toxic, proinflammatory waste-product of improper digestion. We then develop hypotheses and outline preclinical and clinical experiments designed to prove whether “Ama” can serve as a novel and reliable biomarker that links abnormal digestive status, with the onset of chronic inflammation.
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Mariaule, Vincent, Aicha Kriaa, Souha Soussou, Soufien Rhimi, Houda Boudaya, Juan Hernandez, Emmanuelle Maguin, Adam Lesner, and Moez Rhimi. "Digestive Inflammation: Role of Proteolytic Dysregulation." International Journal of Molecular Sciences 22, no. 6 (March 10, 2021): 2817. http://dx.doi.org/10.3390/ijms22062817.

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Dysregulation of the proteolytic balance is often associated with diseases. Serine proteases and matrix metalloproteases are involved in a multitude of biological processes and notably in the inflammatory response. Within the framework of digestive inflammation, several studies have stressed the role of serine proteases and matrix metalloproteases (MMPs) as key actors in its pathogenesis and pointed to the unbalance between these proteases and their respective inhibitors. Substantial efforts have been made in developing new inhibitors, some of which have reached clinical trial phases, notwithstanding that unwanted side effects remain a major issue. However, studies on the proteolytic imbalance and inhibitors conception are directed toward host serine/MMPs proteases revealing a hitherto overlooked factor, the potential contribution of their bacterial counterpart. In this review, we highlight the role of proteolytic imbalance in human digestive inflammation focusing on serine proteases and MMPs and their respective inhibitors considering both host and bacterial origin.
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Balogun, Olugbenga, Cindi R. Brownmiller, Sun-Ok Lee, and Hye Won Kang. "Onion Peel Extract Prevents Intestinal Inflammation via AMK-Activated Protein Kinase Activation in Caco-2/HT-29 Cells." Nutrients 16, no. 21 (October 24, 2024): 3609. http://dx.doi.org/10.3390/nu16213609.

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Background: Obesogenic diets cause intestinal inflammation and dysfunction. Polyphenols have shown a positive impact on reducing inflammation in in vitro studies. However, their bioactivity may not be the same in the in vivo system due to structural alteration by the gastrointestinal digestive process. The purpose of this study was to investigate the anti-inflammatory effect of onion peel and its major bioactive compound, quercetin, in the intestine and further examine the impact of intestinal digestion on this effect. Methods: Onion peel extract (OPE) and quercetin (Q) were digested using gastrointestinal digestive enzymes in vitro and then treated into lipopolysaccharide (LPS)-stimulated Caco-2/HT-29 cells. Genes and proteins related to tight junction, inflammation, and epithelial integrity were measured. Results: OPE and digested OPE (DOPE) had a higher protective effect on LPS-induced tight junction and inflammatory genes and paracellular permeability than Q and digested Q (DQ). DOPE was more effective than OPE, while digestion did not change the activity of Q. The anti-inflammatory effect of OPE and Q with or without digestion was achieved by inhibiting nuclear factor kappa B through AMP-activated protein kinase-activated silent mating-type information regulation 2 homolog 1. Conclusions: It was the first to find that a crude extract, after undergoing gastrointestinal digestion, demonstrated a notably superior anti-inflammatory effect in the cell study, suggesting the consumption of onion peels could potentially yield similar benefits in the human intestine. This discovery underscores the potential of onion peel polyphenols in combating intestinal inflammation, making them a compelling area of research for future therapeutic applications using food byproducts.
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Bourée, Patrice, and Aurélia Lançon. "Blastocystis, pathogène ou simple “indicateur” d’une inflammation digestive ?" Option/Bio 19, no. 398 (April 2008): 16. http://dx.doi.org/10.1016/s0992-5945(08)70098-9.

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Couvineau, Alain, and Cécile Haumaitre. "Special Issue: “Digestive Inflammation and New Therapeutical Targets”." International Journal of Molecular Sciences 25, no. 8 (April 15, 2024): 4361. http://dx.doi.org/10.3390/ijms25084361.

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Nakanishi, Risa, Takahiro Shimizu, Ken Kumagai, Atsushi Takai, and Hiroyuki Marusawa. "Genetic Pathogenesis of Inflammation-Associated Cancers in Digestive Organs." Pathogens 10, no. 4 (April 9, 2021): 453. http://dx.doi.org/10.3390/pathogens10040453.

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Epidemiological, clinical, and biological studies convincingly demonstrate that chronic inflammation predisposes to the development of human cancers. In digestive organs, inflammation-associated cancers include colitis-associated colorectal cancers, Helicobacter pylori-associated gastric cancer, as well as Barrett’s esophagus and esophageal adenocarcinoma associated with chronic duodenogastric-esophageal reflux. Cancer is a genomic disease, and stepwise accumulation of genetic and epigenetic alterations of tumor-related genes leads to the development of tumor cells. Recent genome analyses show that genetic alterations, which are evoked by inflammation, are latently accumulated in inflamed epithelial cells of digestive organs. Production of reactive oxygen and aberrant expression of activation-induced cytidine deaminase, a nucleotide-editing enzyme, could be induced in inflamed gastrointestinal epithelial cells and play a role as a genomic modulator of inflammation-associated carcinogenesis. Understanding the molecular linkage between inflammation and genetic alterations will open up a new field of tumor biology and provide a novel strategy for the prevention of inflammation-associated tumorigenesis.
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Bulgakov, S. A., G. M. Chernakova, E. A. Kleshcheva, and S. V. Simonova. "Comorbid Inflammatory Diseases of Digestive System and Eye." Ophthalmology in Russia 18, no. 1 (April 4, 2021): 20–29. http://dx.doi.org/10.18008/1816-5095-2021-1-20-29.

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Crohn’s disease and ulcerative colitis are chronic inflammatory bowel diseases, which are often accompanied by inflammation of other organs. This article presents modern data on etiology, pathogenesis and clinical course of inflammatory bowel diseases, as well as information on extraintestinal eye manifestations of nonspecific ulcerative colitis and Crohn’s disease. The role of microbiota, genetic factors, immune system defects in pathogenesis of intestinal inflammation and extraintestinal eye manifestations is considered. The possibility the development of ophthalmopathology not only against the background of intestinal inflammation, but also as a consequence of therapeutic and surgical methods of treatment of ulcerative colitis and Crohn’s disease is noted. The peculiarities of the course of episcleritis/scleritis, keratitis, uveitis, chorioretinitis, optical neuritis for patients with inflammatory bowel diseases are considered. The presence of these complications may reflect the activity of the underlying disease, which in some cases requires correction of therapy. Anterior uveitis and episcleritis/scleritis are the most common extraintestinal manifestations of inflammatory bowel disease. Inflammation of tissues of the posterior segment of the eye and optic nerve against the background of ulcerative colitis and Crohn’s disease are less common, but are of clinical importance, as they can catastrophically damage the structures of the eye and, as a consequence, lead to complete blindness. Considering the possibility of mild clinical symptoms and asymptomatic course of inflammation in the eye envelopes, the importance of ophthalmological examination of all patients with ulcerative colitis and Crohn’s disease is emphasized. Aspects of modern therapy of ophthalmopathology and background intestinal inflammation are highlighted. Biological preparations — antagonists of pro-inflammatory cytokines — have been identified as the most promising in the treatment of inflammatory intestinal diseases and extraintestinal manifestations. The important role of proper nutrition and biologically active supplements containing omega-3 fatty acids, vitamin D, microelements, was noted as auxiliary therapy of both intestinal and extraintestinal inflammation.
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YRKM, Sai. "Understanding pancreatic disorders: Acute and chronic pancreatitis, pancreatic cancer and diabetes: A mini-review on a few of the most common pancreatic disorders." Annals of Pancreatic Disorders and Treatment 6, no. 1 (June 29, 2024): 006–10. http://dx.doi.org/10.17352/apdt.000012.

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This mini-review provides an overview of pancreatic disorders, including acute and chronic pancreatitis, pancreatic cancer, and diabetes. The pancreas plays a crucial role in the digestive and endocrine systems of the body, producing enzymes that aid digestion and hormones that regulate blood sugar levels. Acute pancreatitis is a sudden and severe inflammation of the pancreas, often caused by gallstones or excessive alcohol consumption, and requires hospitalization, pain management, and intravenous fluids to support the pancreas. Chronic pancreatitis is a long-term inflammation of the pancreas that may lead to permanent damage and impairment of digestive function. Pancreatic cancer is a malignant tumor that forms in the pancreas and is often difficult to detect and diagnose in its early stages. Treatment for pancreatic cancer may include surgery, chemotherapy, and radiation therapy, depending on the type and stage of the cancer. Diabetes is a metabolic disorder that affects the body’s ability to produce or use insulin, and there are two main types of diabetes: type 1 and type 2. Type 1 diabetes is usually diagnosed in children and young adults and requires lifelong insulin therapy, while type 2 diabetes can often be managed with lifestyle modifications and medication.
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Chang, Ming-Ling, Zinger Yang, and Sien-Sing Yang. "Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression." International Journal of Molecular Sciences 21, no. 21 (November 5, 2020): 8308. http://dx.doi.org/10.3390/ijms21218308.

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Adipose tissue is a highly dynamic endocrine tissue and constitutes a central node in the interorgan crosstalk network through adipokines, which cause pleiotropic effects, including the modulation of angiogenesis, metabolism, and inflammation. Specifically, digestive cancers grow anatomically near adipose tissue. During their interaction with cancer cells, adipocytes are reprogrammed into cancer-associated adipocytes and secrete adipokines to affect tumor cells. Moreover, the liver is the central metabolic hub. Adipose tissue and the liver cooperatively regulate whole-body energy homeostasis via adipokines. Obesity, the excessive accumulation of adipose tissue due to hyperplasia and hypertrophy, is currently considered a global epidemic and is related to low-grade systemic inflammation characterized by altered adipokine regulation. Obesity-related digestive diseases, including gastroesophageal reflux disease, Barrett’s esophagus, esophageal cancer, colon polyps and cancer, non-alcoholic fatty liver disease, viral hepatitis-related diseases, cholelithiasis, gallbladder cancer, cholangiocarcinoma, pancreatic cancer, and diabetes, might cause specific alterations in adipokine profiles. These patterns and associated bases potentially contribute to the identification of prognostic biomarkers and therapeutic approaches for the associated digestive diseases. This review highlights important findings about altered adipokine profiles relevant to digestive diseases, including hepatic, pancreatic, gastrointestinal, and biliary tract diseases, with a perspective on clinical implications and mechanistic explorations.
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Dissertations / Theses on the topic "Digestive inflammation"

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Stevenson, Diane J. "P2X7, inflammation and gastrointestinal disease." Thesis, University of Nottingham, 2008. http://eprints.nottingham.ac.uk/28897/.

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The inflammatory bowel diseases, ulcerative colitis and Crohn's disease are characterised by spontaneously relapsing and remitting inflammation, associated with increased mucosal levels of the inflammatory cytokine, interleukin-1 (IL-1)β. IL-1β processing and release is mediated by ATP stimulation of the purine receptor, P2X7. P2X7 is a membrane ion channel highly expressed in immune cells. Signal transduction occurs via rapid cation exchange, plasma membrane depolarisation and increased intracellular calcium. Additionally, prolonged or repeated P2X7 stimulation leads to formation of a non-selective membrane pore permeable to small molecules, and ultimately to cell death. The aim of this project was to investigate the properties of the P2X7 receptor in mononuclear cells, to show that it is associated with IL-1β release in the colon, and that this release can be modified by P2X7 antagonists. Studies of ethidium bromide uptake, a functional assay, showed that P2X7 receptors are present on LPMCs and displayed properties similar to those of PBMCs and THP-1 cells. P2X7 receptor-stimulation released mature IL-1β from LPMCs in a dose-dependent manner that, in IBD patients, matched the severity of their inflammation, and could be markedly reduced by P2X7 antagonists. P2X7 stimulation also results in increased exposure of phosphatidylserine on the outer cell membrane (PS flip), often considered to be a marker of apoptotic cell death. P2X7-stimulated PS flip however is reversible and is not associated with cell death following brief stimulation times. Cell death caused by longer stimulation did not have features of apoptosis, was more evident in monocytes than lymphocytes, with LPMCs being less susceptible than PBMCs and THP-1 cells. These studies have shown that the P2X7 receptor is intimately involved in the release of IL-1β from human colonic mononuclear cells, that the release is greater in cells from IBD tissue and can be markedly inhibited by P2X7 antagonists.
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Mariaule, Vincent. "Implication des protéases du microbiote intestinal dans les maladies inflammatoires digestives humaines." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASB074.

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Les protéases jouent un rôle clé dans la physiologie humaine en participant à des fonctions essentielles telles que la digestion, l'immunité, la coagulation et la cicatrisation. Cependant, un déséquilibre de la balance protéolytique est également associé à plusieurs maladies y compris les inflammations digestives, des pathologies dont la recrudescence dans le monde est accentuée par l'existence de patients non répondeurs aux traitements actuels. Si l'effet des protéases humaines est actuellement étudié, très peu de données sont disponibles concernant les protéases produites par le microbiote intestinal et leur rôle dans les inflammations digestives. Ce projet de thèse vise à (i) évaluer pour la première fois la contribution des protéases de l'hôte et du microbiote intestinal dans les inflammations digestives, (ii) mener une caractérisation biochimique et cinétique approfondie des protéases candidates et identifier celles présentant des efficacités catalytiques élevées et (iii) valider l'effet délétère de certaines protéases microbiennes et analyser leurs modes d'action in vivo
Proteases play a key role in human physiology in essential functions such as digestion, immunity, coagulation and healing. However, a disequilibrium in proteolytic balance is also associated with several diseases including digestive inflammations, pathologies with high incidence in the world accentuated by the increase of non-responders to available treatments. Although the effect of human proteases is being studied, very little data are available on the proteases produced by the intestinal microbiota and their role in digestive inflammation. This project aims to i) evaluate for the first time the contribution of proteases encoded by the host and intestinal microbiota in digestive inflammations, ii) study the biochemical and kinetic properties of targeted proteases and the identification of those having the highest inhibition efficiencies and iii) validate their deleterious effect and analyze their mode of action in vivo
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Couch, Daniel. "The actions of cannabidiol and palmitoylethanolamide on inflammation and permeability of the gut." Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/51804/.

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In health, the gut provides a barrier between the external and internal environment. This selectively permeable barrier allows absorption of nutrients and water from the gastrointestinal contents, whilst preventing the transfer of noxious material such as bacteria. During episodes of inflammation, this barrier becomes compromised, allowing transfer of noxious material into the systemic circulation, leading to disease states such as inflammatory bowel disease and septic shock. There are no clinically available compounds to combat this increase in permeability directly. The endocannabinoid system is a group of endogenous lipid signalling molecules which activate membrane-bound receptors. Plant-derived and synthetic compounds also act at these receptors, generating a wide variety of secondary effects. The aims of this study were to identify compounds with action on the endocannabinoid system which could be used clinically to treat inflammation and hyperpermeability of the gastrointestinal tract, exploring mechanisms of action. Systematic review and meta-analysis of existing literature revealed 51 preclinical studies, and 2 clinical studies examining the effect of cannabinoid compounds. In preclinical studies, cannabinoid drugs reduced myeloperoxidase activity in the gastrointestinal mucosa within mouse and rodent models of colitis (standard mean difference -1.26, 95% confidence interval (CI)-1.54 to -0.97, I2=48.1%) and macroscopic disease activity scores (standard mean difference -1.36, 95% CI -1.62 to -1.09, I2=61%). Clinical trials found no overall benefit of cannabinoid drugs in Crohn’s disease (mean difference -74.97, 95% CI –229 to 0.79, I2=75%). Two compounds, cannabidiol and palmitoylethanolamide, possessing positive outcomes and preferable side effect profiles, were put forward for further study to examine potential clinical benefit. The mechanism of action of palmitoylethanolamide and cannabidiol were explored further by examination of their effects on the immune response, permeability of cultured cell monolayers, intracellular signalling pathways, expression of membrane-bound proteins governing permeability and receptors of the cannabinoid system. We found that these agents were anti-inflammatory in both cultured Caco-2 cells and explant human colonic tissue, prevented increases in permeability secondary to inflammation, and were likely to act through adenylyl cyclase, protein kinase A and extracellular signal-regulated kinases. The downstream effects of these compounds prevented down-regulation of the TRPV1 receptor, upregulation of aquaporin 3 expression, and prevention of downregulation of claudin-3. The effects of palmitoylethanolamide and cannabidiol were then examined on permeability in the human colon in vivo by means of a double blinded, randomised controlled trial. This study demonstrated that aspirin increased the permeability of the human gut, determined by increases in urinary concentrations of lactulose and D-mannitol, quantified by mass spectrometry. Groups receiving oral cannabidiol or palmitoylethanolamide demonstrated lower urinary concentrations of lactulose and D-mannitol, suggesting that these two drugs could be used clinically to prevent disease-induced hyperpermeability. In conclusion, cannabidiol and palmitoylethanolamide have shown consistent anti-inflammatory actions in colonic ex vivo and in vitro models, and also prevented increases in intestinal permeability in vitro and also in vivo in a randomised, double blind, placebo-controlled trial. Their clinical use in IBD should now be assessed in phase II clinical trials.
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Lamy, Christophe. "Rôle du Corticotropin-Releasing Factor (CRF) périphérique dans les relations stress-inflammation digestive." Université Joseph Fourier (Grenoble), 2003. http://www.theses.fr/2003GRE19020.

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Les maladies inflammatoires cryptogénétiques de l'intestin sont aggravées par le stress. Le but de ce travail est de caractériser le rôle du Corticotropin-Releasing Factor (CRF), neuropeptide clef de la réponse au stress, de son analogue l'urocortine et de leurs récepteurs, CRF1 et CRF2, dans le tube digestif lors d'une colite. L'expression de CRF, urocortine, CRF1 et CRF2 a été localisée par immunohistochimie dans le système nerveux entérique et détectée par RT-PCR quantitative. Il n'éxistait pas de modification du profil d'expression des messagers lors d'une colite à l'acide trinitro-benzènesulfonique (TNBS). Un stress d'immobilisation améliorait la colite après 10 jours et la réactivait après 6 semaines. On observait une tendance à l'augmentation de l'expression du CRF1 et à la diminution de l'expression du CRF2 sous l'effet du stress. En conclusion, le système CRFergique périphérique digestif pourrait expliquer les effets proinflammatoires du stress lors d'une colite
Inflammatory Bowel Disease (IDB) are worsened by stress. The aim of this work was to characterize the role of Corticotropin-Releasing Factor (CRF), a key neuropeptide of the stress response, its analog urocortin and their receptors, CRF1 and CRF2, in the gastro-intestinal tract during colitis. Expression of CRF, urocortin, CRF1 and CRF2 were localized to the enteric nervous system by immunohistochemistry and further detected by quantitative RT-PCR. There was no alteration of the messengers' profile of expression during a trinitrobenzenesulfonique acid (TNBS)-induced colitis. Immobilization stress improved colitis after 10 days and reactivated it after 6 weeks. There was a tendency to an increase in expression of CRF1 and a decrease in expression of CRF2 by stress. In conclusion, digestive peripheral CRF system may account for the proinflammatory of stress effects during colitis
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Charlet, Rogatien. "Rôle des polysaccharides fongiques et du microbiote intestinal dans la clairance digestive de Candida glabrata." Electronic Thesis or Diss., Université de Lille (2022-....), 2022. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2022/2022ULILS025.pdf.

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La maladie de Crohn (MC) est une maladie inflammatoire chronique de l'intestin qui peut s'expliquer par une dysbiose et une dérégulation de la réponse immune chez des individus génétiquement susceptibles. Des observations expérimentales et cliniques suggèrent le rôle prépondérant de certains microorganismes du microbiote intestinal comme agents pouvant contribuer au déclenchement ou au maintien de l'inflammation associée à la MC. Parmi ces derniers, nous retrouvons les levures commensales du genre Candida dont la colonisation digestive est accrue chez les patients atteints de MC. Dans ce contexte, notre équipe étudie le rôle des composants pariétaux fongiques dans la régulation de l'inflammation intestinale. Dans le cas de Candida glabrata (C. glabrata), ces études montrent que la chitine fongique est capable d'atténuer l'inflammation tout en réduisant la prolifération fongique dans un modèle murin de colite chimio-induite. Dans ce même modèle, nous avons montré que la biodiversité bactérienne intestinale se réduit au fur et à mesure du développement de la colite et que cette diminution est corrélée à une augmentation de la prolifération de C. glabrata. De plus, l'ajout de la chitine a pour conséquence de modifier le microbiote intestinal en faveur des bactéries anaérobies : Bacteroides thetaiotaomicron et Lactobacillus johnsonii. Par la suite et dans ce même modèle, l'administration orale de ces deux bactéries anaérobies ont permis de révéler que celles-ci participent au même titre que la chitine à l'atténuation de l'inflammation intestinale et à la réduction des populations pathobiontes.Toutefois, les mécanismes qui régissent l'interaction Candida-bactéries anaérobies ainsi que les déterminants moléculaires mis en jeu restent à caractériser. La première partie de ce projet a été d'étudier les métabolites impliqués dans l'interaction bactéries anaérobies- cellules épithéliales intestinales coliques de souris. Nos études montrent que l'acide oléique (OA), seul ou combiné avec l'acide palmitique (PA), présente des propriétés anti-inflammatoires notables en réduisant l'expression de plusieurs marqueurs inflammatoires exprimés par les cellules Caco-2 exposées au DSS (Dextran sulfate de sodium). Nos investigations ont également démontré que l'activité de l'OA sur les macrophages induirait une augmentation de l'expression de l'IL-10 et une diminution de divers marqueurs pro-inflammatoires, probablement en lien avec la reconnaissance de l'OA par les récepteurs FFARs et AhR. Ces AG présentent aussi des propriétés inhibitrices sur la formation du biofilm, l'adhérence et la viabilité fongique. L'ensemble de ces propriétés a été confirmé dans un modèle murin de colite DSS-induite où l'administration orale de ces deux AG atténue les paramètres inflammatoires tout en réduisant la prolifération de C. glabrata et des populations bactériennes pathobiontes.Dans la seconde partie de ce projet, nos investigations confirment les propriétés anti-inflammatoires et immunomodulatrices de la chitine administrée de manière curative (par voie intra-péritonéale) à des souris avec colite DSS-induite. Ce traitement induit une diminution des paramètres inflammatoires (scores clinique et histologique), de l'expression des cytokines et médiateurs pro-inflammatoires conduisant à une diminution des charges fongique et bactérienne aérobie fécales. Les souris, prétraitées avec de la chitine (administrée par voie sous-cutanée) préalablement à leur exposition au DSS, sont protégées contre la colonisation digestive par C. glabrata. Bien qu'il s'agisse d'un résultat déterminant, les mécanismes qui régissent la clairance fongique associés à ce traitement restent encore à explorer. Nos données montrent aussi que ce traitement préventif permet d'induire des anticorps dirigés contre la chitine. Cependant et contrairement au traitement curatif, ce traitement ne permet pas de réduire l'inflammation intestinale
Crohn's disease (CD) is a chronic inflammatory disease of the intestine caused by dysbiosis and dysregulation of the immune response in genetically-susceptible individuals. Experimental and clinical studies suggest that certain microorganisms in the intestinal microbiota play a major role in the triggering or maintenance of inflammation associated with CD. These microorganisms include commensal yeasts of the genus Candida, which increase significantly in the digestive tract of patients with CD. In this context, our group studied the role of fungal cell wall components in the regulation of intestinal inflammation. In the case of Candida glabrata, these studies showed that fungal chitin is capable of attenuating inflammation while reducing fungal proliferation in a murine model of chemically-induced colitis. In this same model, we also showed that the intestinal bacterial biodiversity decreases gradually as colitis develops and that this decrease is correlated with an increase in proliferation of C. glabrata. In addition, the addition of chitin modifies the intestinal microbiota in favour of the anaerobic bacteria Bacteroides thetaiotaomicron and Lactobacillus johnsonii. As a result, and in this same model, oral administration of these two anaerobic bacteria revealed that they participate in the same way as chitin in the attenuation of intestinal inflammation and the reduction of disease-causing populations.However, the mechanisms that regulate the interaction between Candida and anaerobic bacteria, as well as the molecular determinants brought into play, remain to be characterised. The first part of our work studied the metabolites involved in the interaction between anaerobic bacteria and colonic epithelial cells of mice. These studies showed that oleic acid (OA), alone or combined with palmitic acid (PA), had notable anti-inflammatory properties by reducing the expression of several inflammatory markers expressed by Caco-2 cells exposed to DSS (dextran-sulphate sodium). Our investigations also demonstrated that the action of OA on macrophages induced an increase in expression of IL-10 and a decrease in diverse pro-inflammatory markers, probably linked to the recognition of OA by the receptors FFARs and AhR. These fatty acids also had inhibitory properties on biofilm formation, adherence and fungal viability. All of these properties were confirmed in a murine model of DSS-induced colitis where the oral administration of these two fatty acids attenuated inflammation by reducing the proliferation of C. glabrata and disease-causing bacterial populations.In the second part of this project, our investigations confirmed the anti-inflammatory and immunomodulating properties of chitin administered curatively (by intra-peritoneal administration) to mice with DSS-induced colitis. This treatment induced a decrease in inflammatory parameters (clinical and histological scores) and the expression of cytokines and pro-inflammatory mediators, leading to a decrease in the fungal and aerobic bacterial load in the faeces. Mice, pretreated with chitin (administered subcutaneously) prior to their exposure to DSS, were protected against digestive colonisation by C. glabrata. Although this is a significant result, the mechanisms that lead to fungal clearance associated with this treatment are unknown. Our data show that this preventive treatment induces antibodies directed against chitin. However, and contrary to curative treatment, this treatment does not reduce intestinal inflammation
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Péré-Védrenne, Christelle. "Etude de la Cytolethal Distending Toxin B des Hélicobacters dans l’inflammation et la carcinogenèse digestive." Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0404/document.

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La démonstration du rôle de la CDT (« Cytolethal Distending Toxin ») de Helicobacterhepaticus dans le développement de l’hépatocarcinome murin fait de cette toxine un candidatpertinent dans l'activation de processus pro-cancéreux. Comme la toxine CagA de Helicobacterpylori, la sous-unité active CdtB de la CDT pourrait être une oncoprotéine. Nous avons étudié lerôle de la CdtB des Hélicobacters dans l’inflammation et la carcinogenèse digestive via unestratégie lentivirale d’expression constitutive ou conditionnelle de la CdtB ou de son mutant pourl’activité DNase. Nous avons réalisé une étude du transcriptome et montré que la CdtB deH. hepaticus induisait une réponse inflammatoire en surexprimant des cytokines, chimiokines,peptides antimicrobiens et en activant la voie du NF-κB des cellules épithéliales. La CdtB réguleégalement l’expression et la localisation nucléaire du facteur de transcription et oncogène MafB.Ces résultats ont été confirmés pour la CdtB de Helicobacter pullorum. Des expériencesd'infection des cellules avec des souches sauvages et mutées pour la CDT (deH. hepaticus & H. pullorum) ont permis de valider les résultats obtenus et de les attribuer à laCdtB et notamment à son activité DNase. Nous avons aussi développé un nouveau modèle dexénogreffes de cellules épithéliales inductibles pour l’expression de la CdtB de H. hepaticus.Dans ce modèle, la CdtB, en plus de ses effets déjà connus, retarde la croissance tumorale,induit l’apoptose, la sénescence et la surexpression du marqueur nucléaire de prolifération,Ki-67, suggérant la survie cellulaire. L’ensemble de ces résultats fournit de nouveaux argumentsen faveur du potentiel oncogénique de la CDT
The demonstration of the role of the Cytolethal Distending Toxin (CDT) of Helicobacter hepaticusin the development of hepatocarcinoma in mice, makes this toxin a relevant candidate in theactivation of precancerous processes. As in the case of the CagA toxin of Helicobacter pylori, theCdtB active subunit of CDT could be an oncoprotein. We studied the role of Helicobacter CdtB ininflammation and digestive carcinogenesis using a lentiviral strategy for constitutive or conditionalexpression of the CdtB subunit or its corresponding DNase mutant. We conducted a study of thetranscriptome and showed that CdtB induced an inflammatory response by overexpressingcytokines, chemokines, antimicrobial peptides and activating the NF-kB pathway in epithelialcells. The CdtB also regulated the expression and nuclear localization of the transcription factorand oncogene MafB. These results were confirmed for the CdtB of Helicobacter pullorum.Infection of cells with wild type strains and the corresponding CDT-mutant strains (of H. hepaticus& H. pullorum) were used to validate the results and to attribute the effects to the CdtB and, inparticular, to its DNase activity. We also developed a novel epithelial cell xenograft model toevaluate the inducible expression of H. hepaticus CdtB. In this model, the CdtB, in addition to itspreviously well-known effects, delayed tumor growth, induced apoptosis, senescence and theoverexpression of nuclear proliferation marker, Ki-67, suggesting cell survival. All of these resultsprovide new arguments in favor of the oncogenic potential of the CDT
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Kimse, Moussa. "Caractérisation de l'écosystème cæcal et santé digestive du lapin : contrôle nutritionnel et interaction avec la levure probiotique saccharomyces cerevisiae." Thesis, Toulouse, INPT, 2009. http://www.theses.fr/2009INPT001A/document.

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L’écosystème digestif est sous l’influence de facteurs abiotiques et biotiques qui déterminent son équilibre et par conséquent influencent la santé digestive de l'hôte. Chez le lapin en croissance, un déséquilibre de l’écosystème caecal est associé aux entéropathies, responsables de mortalités importantes en élevage. La compréhension des interactions biotope – biocénose digestive permettra la mise en oeuvre de stratégies pour garantir l'équilibre de cet écosystème. Ainsi, le rôle des facteurs biotiques de stabilité l’écosystème digestif, tels que des microorganismes exogènes probiotiques, fait actuellement l’objet de nombreuses études, mais leur mode d’action sur la biocénose et le biotope reste encore peu clair. L’objectif de notre travail est de contribuer à la compréhension du fonctionnement de l'écosystème caecal chez le jeune lapin, soumis ou non à un stress nutritionnel et en présence ou non d'une flore exogène ajoutée. Il s'agit aussi, de faire une approche comparative des effets d'un même probiotique (S. cerevisiae) dans cet écosystème et dans le rumen de la vache, pour mieux décrire les mécanismes d'action d'une levure probiotique sur les relations biocénose-biotope. Dans ce but, nous avons mis au point et validé pour le caecum du lapin la mesure du potentiel redox (Eh), pour mieux juger de l'état d'anaérobiose du biotope caecal. Nous avons également validé un nouvel indicateur de l’inflammation générale (haptoglobine sérique) en réponse à l'application d'un stress nutritionnel ou d'un état sanitaire déficient. Comparé au rumen, le biotope caecal est un milieu très anaérobie, puisque son potentiel redox moyen est de -220 mV et ne varie pas avec l’âge (de 28 à 64 jours). La biodiversité de la biocénose bactérienne caecale, calculée à partir de leur empreinte moléculaire (CE-SSCP) est en moyenne de 5,0 (indice de Simpson). Chez l'animal touché par un dysfonctionnement digestif, nous observons une élévation du niveau général de l'inflammation (+70% du taux d’haptoglobine sérique), associée à une chute de l'activité fermentaire caecal (-50%) et une hausse du pH (+ 0,7), mais qui n'est pas associée à des variations d'Eh caecal ou de la diversité bactérienne. L'application d'un stress nutritionnel (déficience en fibres) entraîne chez le lapin une baisse de la concentration caecale en AGV totaux (-25%) et une hausse du pH (+0,1). Cependant, la déficience en fibres n’a pas d'effet marqué sur le Eh caecal, dont la moyenne est de -210 mV. De même, la diversité bactérienne n’est pas modifiée (5,3) par la réduction de la teneur en fibres de l’aliment et la similarité observée est de 76%. La teneur de fibres dans l’aliment n’influence pas non plus le niveau d'inflammation générale. L’apport de levures vivantes dans la ration du lapin tend à augmenter la diversité bactérienne (+10%), et peut élever le potentiel redox caecal de 25 mV caecal. Il n’affecte cependant pas la structure du microbiote bactérien caecal (similarité= 99%). Elle n’entraîne pas non plus de variation du taux d’haptoglobine. L'ingestion de levures vivantes a permis l’amélioration de la santé digestive par la réduction de la mortalité (jusqu'à -50%) pendant les périodes de forte mortalité où le taux d’haptoglobine sérique augmente d’environ 70%. L’effet de la levure observé ici dans le caecum du lapin diffère de celui observé dans le rumen de la vache, pour lequel on observe une baisse du potentiel redox et une hausse du pH, ce qui favoriserait l’activité des bactéries anaérobies strict transformant le lactate en propionate. La levure stabiliserait donc le biotope (pH, potentiel redox) qui favoriserait la croissance ou l’activité de certaines bactéries. Cette hypothèse reste encore à confirmer pour l'écosystème caecal du lapin, à l'aide méthode appropriées
The digestive ecosystem is influenced by abiotics and biotics factors that determined its balance and consequently influenced the host digestive health. In the young rabbit, caecal ecosystem disorders are largely responsible for nonspecific enteropathies that cause livestock losses. Understanding biotope/biocenosis interrelationships would allow the development of new strategies that preserve the ecosystem balance. Thus, the role of biotic factors that stabilise the digestive ecosystem, such as probiotics is extensively studied, however their effects on biocenosis and biotope remain unclear. The aim of our work is to improve our understanding of the caecal ecosystem functioning, submitted or not to a nutritional stress and with or without addition of an exogenous flora. We also aimed to compare the effects of the same probiotic (S. cerevisiae) in the caecum and in the rumen (dairy cow), to improve our knowledge on the mechanisms of action of yeast probiotic on biocenosis and biotope. We have developed and validated the measure of redox potential in the caecum. We also validated for the growing rabbit, a new indicator of the general inflammation (haptoglobin) in response to the application of nutritional stress or under a deficient sanitary status. Compared to the rumen, the caecal biotope is very anaerobic, since its redox potential is meanly of -220mV, and do not vary with age (35-63d old). The biodiversity of the bacterial community in the caecum, calculated from fingerprint technique (SSCP), reached meanly 5.0 (Simpson index). In the rabbit having a digestive trouble, the seric haptoglobin concentration increased by 70%, while caecal fermentative activity dropped by 50%. In parallel, the caecal pH increased (+0,7 unit) whereas the redox potential and the bacterial diversity remain unaffected in the caecum. When the young rabbit is submitted to a nutritional stress (fibre deficiency), the caecal volatile fatty acids concentration dropped by 25%, while the pH increased by 0.1 unit. However, the fibre deficiency did not affect the caecal redox potential (meanly -210 mV). Similarly, the bacterial biodiversity in the caecum was not modified (5,3) according to dietary fibre intake, as well the bacterial community structure. Besides, the haptoglobin concentration remained similar with fibre intake. The live yeast added in the diet tended to increase the bacterial diversity (+10%), and could slightly increase the caecal Eh (+25 mV). Yeast have no effect on the structure of rabbit caecal microbiota (bacteria only), where the similarity is 99%. It does not change the serum haptoglobin level. In return, yeast addition improved the digestive health by reducing mortality rate by 50%, particularly during periods of high mortality, when the serum haptoglobin increased by 70%. The effect of yeast described in the rabbit caecum differed from that found for the cow rumen: yeast decreased the redox potential and increased the pH that favors the strict anaerobic bacterial activity. The live yeast thus would stabilise the biotope (pH, Eh) and would favor the growth and activity of specific bacteria. However, this hypothesis still remains to be confirmed for the rabbit caecal ecosystem, using pertinent methodology
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Fulham, Melissa A. "Characterization of Adipose Tissue Inflammation in Alcoholic Liver Disease." eScholarship@UMMS, 2011. http://escholarship.umassmed.edu/gsbs_diss/940.

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Adipose tissue inflammation has an impact on liver health and it has been demonstrated that chronic alcohol consumption leads to the expression of pro-inflammatory markers in the adipose tissue. A thorough characterization of alcohol-induced adipose inflammation is lacking, and is important to understand in order to identify immune-related mechanisms that drive this phenomenon. Current therapeutic regimens for alcoholic liver disease are ineffective. It is critical to understand how other organs influence liver injury in this disease when developing novel and effective therapies in the future. Alcoholic liver disease exhibits a sexual dimorphism; women are more susceptible to liver injury than men and the same paradigm exists in rodent models. Here, I demonstrate that female mice have greater alcohol-induced adipose tissue inflammation than male mice, evidenced by greater expression of pro-inflammatory cytokines and cell markers. Further, female mice also exhibit higher expression of toll-like receptor genes in the adipose tissue, suggesting a potential role for the innate immune system in alcohol-induced adipose inflammation. Toll-like receptor 4 (TLR4) has been demonstrated to drive inflammation in both the liver and adipose tissue. I used both germline and conditional knockouts of Tlr4 to characterize alcohol-induced changes in the immune cell composition of adipose tissue. Alcohol increased the number of pro-inflammatory adipose tissue macrophages. This macrophage phenotype switching is partially dependent on TLR4; germline, but not myeloid-specific, Tlr4-deletion prevents macrophage phenotype switching. Overall, my work demonstrates that alcohol-induced adipose tissue inflammation is related to liver injury and that TLR4 contributes to adipose macrophage phenotype switching.
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Fulham, Melissa A. "Characterization of Adipose Tissue Inflammation in Alcoholic Liver Disease." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/940.

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Adipose tissue inflammation has an impact on liver health and it has been demonstrated that chronic alcohol consumption leads to the expression of pro-inflammatory markers in the adipose tissue. A thorough characterization of alcohol-induced adipose inflammation is lacking, and is important to understand in order to identify immune-related mechanisms that drive this phenomenon. Current therapeutic regimens for alcoholic liver disease are ineffective. It is critical to understand how other organs influence liver injury in this disease when developing novel and effective therapies in the future. Alcoholic liver disease exhibits a sexual dimorphism; women are more susceptible to liver injury than men and the same paradigm exists in rodent models. Here, I demonstrate that female mice have greater alcohol-induced adipose tissue inflammation than male mice, evidenced by greater expression of pro-inflammatory cytokines and cell markers. Further, female mice also exhibit higher expression of toll-like receptor genes in the adipose tissue, suggesting a potential role for the innate immune system in alcohol-induced adipose inflammation. Toll-like receptor 4 (TLR4) has been demonstrated to drive inflammation in both the liver and adipose tissue. I used both germline and conditional knockouts of Tlr4 to characterize alcohol-induced changes in the immune cell composition of adipose tissue. Alcohol increased the number of pro-inflammatory adipose tissue macrophages. This macrophage phenotype switching is partially dependent on TLR4; germline, but not myeloid-specific, Tlr4-deletion prevents macrophage phenotype switching. Overall, my work demonstrates that alcohol-induced adipose tissue inflammation is related to liver injury and that TLR4 contributes to adipose macrophage phenotype switching.
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Davis, Laura D. R. "The Biodistribution of 14C in the Digestive Organs of Rats Fed [14C]CD14 Protein." Thesis, Université d'Ottawa / University of Ottawa, 2010. http://hdl.handle.net/10393/12911.

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Human milk contains ~ 25 µg/mL of soluble cluster of differentiation 14 (sCD14) protein, a pattern recognition receptor (PRR) that triggers the innate immune system to respond to bacterial lipopolysaccharide (LPS). To date, the role of CD14 in the digestive tract of breast fed infants has not been well characterized and is the subject of this thesis. To investigate the biodistribution of proteins such as CD14 in vivo, a novel method for 14C radiolabeling of proteins to high specific radioactivity was developed using in vacuo methylation. Bovine serum albumin (BSA) and casein were used as test proteins to determine the following: 1) The efficacy of the in vacuo radiolabeling procedure; 2) The extent of incorporation of the 14C-label into the organs of oro-gastric gavaged 10 day old Sprague Dawley rats. [14C]BSA, [14C]casein and [14C]CD14 were prepared with specific radioactivities of 10 400, 10 800 and 163 000 dpm/µg, respectively. After feeding 6.25 µg of 14C-labeled proteins, quantifiable levels of 14C were found in the stomach, jejunum, duodenum, ileum, large intestine, intestinal luminal flushes, blood, liver, spleen and kidneys of rats. The accumulation of radiolabel in the organs of [14C]CD14 fed rats was temporally and spatially distinct from [14C]BSA and [14C]casein. Most notably, the label persisted in the stomach 480 min post-gavage. To design a neonate animal model for biodistribution, the segmental and total gastrointestinal transit times (GItt) were measured in two litters of 10 and 15 day old Sprague Dawley rat pups using barium sulfate. Ten day old rat pups that remained with and without the dam had a total gastrointestinal transit time of 13.8 ± 0.9 hr and 9.3 ± 0.7 hr, respectively. This decrease (p<0.05) in total gastrointestinal transit time in the absence of the dam was age dependent, as it was not observed (p>0.05) in the 15 day old rat pup litter. The immunological impact of an exogenous sCD14 source was examined in human peripheral blood mononuclear cells (PBMC). Pre-treatment of CD14+ monocytes with sCD14 had a protective effect, one of reducing the production of proinflammatory cytokines (TNF-α, IL-6, IL-8, IL-1β) when challenged with LPS. 14C was absorbed by neonate rats upon ingestion of [14C]CD14 and exposure to relatively high concentrations of rCD14 led to a reduction in inflammation. This may be beneficial to initial gut colonization in breast-fed newborns.
Alexander Graham Bell NSERC CGS M scholarship. Japan Society for the Promotion of Sciences, Summer in Japan Fellowship. Funded by the Canadian Institutes of Health Research, Institute of Nutrition Metabolism and Diabetes Grant #82816 “Fate and function of breast milk and recombinant human CD14 at mammary and newborn gastrointestinal mucosal epithelia”.
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Books on the topic "Digestive inflammation"

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Falk, Symposium (173rd 2010 Brno Czech Republic). From chronic inflammation to cancer: Falk Symposium 173, June 4-5, 2010, Brno. Basel: Karger, 2010.

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Julia, Mayerle, and Tilg Herbert, eds. Clinical update on inflammatory disorders of the gastrointestinal tract. Basel: Karger, 2010.

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Julia, Mayerle, and Tilg Herbert, eds. Clinical update on inflammatory disorders of the gastrointestinal tract. Basel [Switzerland]: Karger, 2010.

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Herbert, Tilg, and Mayerle Julia, eds. Clinical update on inflammatory disorders of the gastrointestinal tract. Basel: Karger, 2010.

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A, Stallmach, ed. Induction and modulation of gastrointestinal inflammation: Proceedings of the Falk Symposium 104 held in Saarbrücken, Germany, March 5-7, 1998. Dordrecht: Kluwer Academic Publishers, 1999.

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R, Mahida Y., ed. Immunological aspects of gastroenterology. Dordrecht: Kluwer Academic Publishers, 2001.

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G, Holtmann, and Talley Nicholas Joseph, eds. Gastrointestinal inflammation and disturbed gut function: The challenge of new concepts : proceedings of Falk Symposium 130 (part I of the Gastroenterology Week, Freiburg 2002) held in Freiburg, Germany October 4-6, 2002. Dordrecht: Kluwer Academic, 2003.

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Novak, Bull Lorena, ed. The everything coconut diet cookbook: The delicious and natural way to lose weight fast, boost energy, improve digestion, reduce inflammation, and get healthy for life. Avon, Mass: Adams Media, 2012.

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Pharmacotherapy of Gastrointestinal Inflammation (Progress in Inflammation Research). Birkhäuser Basel, 2004.

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Waldmann, Carl, Neil Soni, and Andrew Rhodes. Infection and inflammation. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0027.

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Pathophysiology of sepsis and multi-organ failure 462Infection control—general principles 464HIV 466Severe falciparum malaria 468Vasculitides in the ICU 470Source control 472Selective decontamination of the digestive tract (SDD) 474Markers of infection 476Adrenal insufficiency and sepsis 478Infectious agents entering the body lead to local inflammation, pus and abscess formation, and affect the whole body through systemic inflammation. Systemic inflammation is recognized by the presence of fever, abnormal WCC, and increased heart and respiratory rate, and is known as systemic inflammatory response syndrome (SIRS). If SIRS is due to infection (as distinct from other causes such as pancreatitis, burns or major trauma) it is defined as sepsis....
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Book chapters on the topic "Digestive inflammation"

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Spencer, A. J., Raymond Everett, and James A. Popp. "Multifocal Inflammation, Liver, Rat." In Digestive System, 217–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60473-7_32.

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Spencer, A. J., Raymond Everett, and James A. Popp. "Multifocal Inflammation, Liver, Rat." In Digestive System, 217–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-25996-2_32.

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Rommes, Hans, Rick van Saene, and Miguel A. de la Cal. "Inflammation and Hyperinflammation." In Selective Decontamination of the Digestive Tract (SDD), 233–43. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65225-8_16.

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Naito, Y., and T. Yoshikawa. "Neutrophil-Dependent Oxidative Stress in Gastrointestinal Inflammation." In Oxidative Stress and Digestive Diseases, 24–40. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062727.

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Gunes Kocinkag, Vezire, and Muhammed Kocinkag. "Medical Use of Cardamom (Elettaria Cardamomum L.)." In Medicinal Spices, 239–46. Istanbul: Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359340.15.

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Cardamom (Elettaria cardamomum L.) is a spice that is widely used especially in Asian cuisine and is also valuable for medicinal purposes. Thanks to the active ingredients it contains, Cardamom supports digestive health and can relieve stomach discomfort. Additionally, it has antioxidant properties and can reduce inflammation, thus having anti-inflammatory effects. Some research shows that cardamom has the ability to balance blood sugar levels, suggesting it may play a potential role in diabetes management. Additionally, cardamom has antimicrobial properties and can therefore be used to support oral health.
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Deniz, Gulnihal, and Derya Ozturk Soylemez. "The Small Intestine." In Clinical Anatomy of Digestive System a Handbook for Healthcare Professionals, 91–123. Istanbul: Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053358855.5.

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This section provides a comprehensive overview of the duodenum, jejunum, and ileum, focusing on their anatomical characteristics, vascularization, innervation, and clinical relevance. The duodenum, the initial segment of the small intestine, is divided into four parts: superior, descending, inferior, and ascending. The inner surface of the duodenum features numerous folds and villi that increase its surface area for nutrient absorption. Its wall structure comprises several layers, including the mucosa, submucosa, muscularis, and serosa. The arterial supply to the duodenum includes branches from the Right gastric artery, Supraduodenal artery, Right gastro-omental artery, superior pancreaticoduodenal artery, and inferior pancreaticoduodenal artery. Venous drainage from the duodenum occurs through the splenic (lienal), Superior mesenteric, and Hepatic portal veins. Lymphatic drainage follows a similar path, with lymph nodes along the arteries. Neural innervation of the duodenum involves the sympathetic and parasympathetic nervous systems, facilitating the regulation of digestive processes. Clinically, conditions such as duodenal ulcers and obstructions are common issues affecting the duodenum, necessitating a thorough understanding of its anatomy for effective diagnosis and treatment. Moving to the jejunum and ileum, this section highlights the differences between these two parts of the small intestine. The jejunum, which follows the duodenum, is characterized by a thicker wall, larger diameter, and more prominent circular folds than the ileum. The ileum, the final part of the small intestine, has a thinner wall, smaller diameter, and fewer circular folds. It also features Peyer’s patches, lymphoid tissues crucial for immune function. The mesentery, a fold of the peritoneum, supports the jejunum and ileum, providing a conduit for blood vessels, nerves, and lymphatics. A notable clinical condition associated with the ileum is the ileal diverticulum (Meckel’s diverticulum), a congenital anomaly that can lead to complications such as bleeding or inflammation. The wall structure of the small intestine is similar to that of the duodenum, with adaptations that facilitate absorption. Circular folds, or plicae circulares, are prominent in the jejunum and gradually diminish towards the ileum, vital in increasing the surface area for nutrient absorption. In clinical practice, understanding the anatomical and functional distinctions between the jejunum and ileum and their common pathologies is essential for accurate diagnosis and effective management of gastrointestinal disorders.
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Spanos, Constantine P. "Inflammation and digestive malignancies." In Digestive System Malignancies, 87–92. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-98369-3.00014-9.

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Waldmann, Carl, Andrew Rhodes, Neil Soni, and Jonathan Handy. "Infection and inflammation." In Oxford Desk Reference: Critical Care, 503–22. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198723561.003.0028.

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This chapter discusses infection and inflammation and includes discussion on the general principles of infection control (involving discussion on ventilator-associated pneumonia, urinary catheters, antimicrobial stewardship and resistance, and prevention of transmission of infection), human immunodeficiency virus (HIV; HIV testing in the critical care setting, antiretroviral therapy in the critically ill patient, Pneumocystis jiroveci pneumonia, cryptococcal meningitis, and toxoplasmosis encephalitis), severe falciparum malaria, vasculitides in the intensive care unit, source control (prophylaxis, antibiotics, abscess, necrotic tissue, and infected foreign body), selective decontamination of the digestive tract (including discussion on theory, potential pathogenic microorganisms, and typical protocol), markers of infection, and adrenal insufficiency and sepsis.
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Carlos, Gustavo Campanha Menon, Camilla Martins Ginack, Giovanna Iemini Costa, Lucas Martins Ribeiro Ferreira, Antônio Duarte Cabral, Isabella Moreira Alves de Souza, and Ethel Zimberg Chehter. "Treatment for Eosinophilic Esophagitis in adults: where are we?" In DEVELOPMENT AND ITS APPLICATIONS IN SCIENTIFIC KNOWLEDGE. Seven Editora, 2023. http://dx.doi.org/10.56238/devopinterscie-150.

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(1) Eosinophilic Esophagitis (EEo) is a disease that falls within a spectrum of eosinophilic gastrointestinal disorders, the inflammation of which has no secondary causes. (2) EEo is defined as a chronic, inflammatory, antigen-mediated esophageal disease, which can be characterized by clinical symptoms related to esophageal dysfunction, (3) such as dysphagia, vomiting, and food impact (2) and by histology compatible with predominant inflammation of eosinophils. (3) Diagnostic confirmation is confirmed with the presence of 15 or more eosinophils per highly increased field in esophageal biopsies performed via upper digestive endoscopy (EDA) and the absence of eosinophilic infiltrate in the other segments of the digestive tract.
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Carlos, Gustavo Campanha Menon, Camilla Martins Ginack, Giovanna Iemini Costa, Lucas Martins Ribeiro Ferreira, Antônio Duarte Cabral, Isabella Moreira Alves de Souza, and Ethel Zimberg Chehter. "Treatment for Eosinophilic Esophagitis in adults: Where are we?" In DEVELOPMENT AND ITS APPLICATIONS IN SCIENTIFIC KNOWLEDGE. Seven Editora, 2023. http://dx.doi.org/10.56238/devopinterscie-146.

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(1) Eosinophilic Esophagitis (EEo) is a disease that falls within a spectrum of eosinophilic gastrointestinal disorders, the inflammation of which has no secondary causes. (2) EEo is defined as a chronic, inflammatory, antigen-mediated esophageal disease, which can be characterized by clinical symptoms related to esophageal dysfunction, (3) such as dysphagia, vomiting, and food impact (2) and by histology compatible with predominant inflammation of eosinophils. (3) Diagnostic confirmation is confirmed with the presence of 15 or more eosinophils per highly increased field in esophageal biopsies performed via upper digestive endoscopy (EDA) and the absence of eosinophilic infiltrate in the other segments of the digestive tract.
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Conference papers on the topic "Digestive inflammation"

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Pyne, Ashley L. "Food-Specific Antibodies Reflect Inflammation and Antigen Removal in Eosinophilic Esophagitis." In World Congress of Gastroenterology and Digestive Diseases, 75. United Research Forum, 2024. https://doi.org/10.51219/urforum.2024.ashley-l-pyne.

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Liu, Chang, Wu-ran Wei, Jun-he Gou, Jia-yin Yang, Hua Du, Tian-Fu Wen, Li Jiang, and Wu-sheng Lu. "Prognostic Value of Inflammation Scores in Liver Cancer Post Transarterial Chemoembolization." In 4th Annual Meeting of the American Society of Digestive Disease Interventions. Thieme Medical Publishers, 2017. http://dx.doi.org/10.1055/s-0038-1641647.

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Liu, Chang, Bo Yuan, Jia-yin Yang, Hua Du, Lu-nan Yan, Li Jiang, Tian-fu Wen, et al. "Combined Inflammation-based Index Predicts Outcomes of Hepatocellular Carcinoma Treated with Transarterial Embolization." In 4th Annual Meeting of the American Society of Digestive Disease Interventions. Thieme Medical Publishers, 2017. http://dx.doi.org/10.1055/s-0038-1641645.

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Zhou, Gaoshi. "IDDF2018-ABS-0230 Transglutaminase 2 modulates inflammation-associated angiogenesis via VEGFR2 pathway in crohn’s disease." In International Digestive Disease Forum (IDDF) 2018, Hong Kong, 9–10 June 2018. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-iddfabstracts.33.

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Zhao, Hailan, Yao Peng, Jing Xu, Haoming Xu, Wenqi Huang, Jiaqi Wang, Xue Guo, et al. "IDDF2021-ABS-0200 Bacillus amyloliquefaciens combined with resistant starch to ameliorate intestinal inflammation." In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 4–5 September 2021. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2021. http://dx.doi.org/10.1136/gutjnl-2021-iddf.58.

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Tsai, Kun Yu, and Wen Sy Tsai. "IDDF2018-ABS-0172 Dietary factor related to ulcerative colitis inflammation. avoidance of factor could benefit disease control?" In International Digestive Disease Forum (IDDF) 2018, Hong Kong, 9–10 June 2018. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-iddfabstracts.139.

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Wang, Yifei, Kaiyu Sun, Jingxian Shen, Bin Li, Qinghua Cao, Sui Peng, and Ming Kuang. "IDDF2019-ABS-0066 Novel prognostic nomograms based on inflammation-related markers for patients with hepatocellular carcinoma underwent hepatectomy." In International Digestive Disease Forum (IDDF) 2019, Hong Kong, 8–9 June 2019. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-iddfabstracts.252.

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Ho, Cheng-Maw, Shu-Li Ho, Yu-Sheng Lai, Shao-Chun Lu, Hui-Ling Chen, Po-Yuan Chang, Rey-Heng Hu, and Po-Huang Lee. "IDDF2019-ABS-0081 Portal free cholesterol and oxidized-LDL accumulation is associated with plaque formation and inflammation in human NAFLD." In International Digestive Disease Forum (IDDF) 2019, Hong Kong, 8–9 June 2019. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-iddfabstracts.88.

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Chen, Wei, Jinshui Zhu, Jing Zhang, Rui Liang, Youcai Yi, Xiaoyu Chen, and Huining Fan. "IDDF2021-ABS-0097 P38α deficiency in macrophages ameliorates murine experimental colitis by regulating inflammation and immune process." In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 4–5 September 2021. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2021. http://dx.doi.org/10.1136/gutjnl-2021-iddf.34.

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Jiang, Dianxuan, Songfeng Chen, Qianjun Zhuang, Niandi Tan, and Mengyu Zhang. "IDDF2024-ABS-0314 Lipopolysaccharide leads to inflammation and impairment of esophageal epithelial barrier and causes reflux symptoms." In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 10 – 11 August 2024, A198—A201. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2024. http://dx.doi.org/10.1136/gutjnl-2024-iddf.124.

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Reports on the topic "Digestive inflammation"

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Yu, Dongli, Jingting Liu, Chunyan Meng, Baoqing Liu, and Jianhua Liao. Pan-immune-inflammation value as a Novel Prognostic Biomarker for Digestive System Cancers: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2024. http://dx.doi.org/10.37766/inplasy2024.9.0087.

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You might also be interested in the extended bibliographies on the topic 'Digestive inflammation' for particular source types:
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