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The patient with acute gastrointestinal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Rebecca Maindonald, Adrian Jugdoyal
The Kupffer cells are phagocytic and are very efficient in digesting bacteria, viruses and other foreign matter. These cells are particularly important because they destroy bacteria that are constantly entering the portal blood flow directly from the GI tract. The main functions of Kupffer cells are: phagocytosis of bacteria, debris and other foreign matter in hepatic blood.a defence mechanism when bacterial translocation occurs.
Infections in Cirrhosis in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
John M. Horne, Laurel C. Preheim
Because enteric bacteria predominate in SBP, it is thought that the gut is the major source of organisms for this infection. Several mechanisms have been proposed to explain the movement of organisms from the intestinal lumen to the systemic circulation. Cirrhosis-induced depression of the hepatic reticuloendothelial system impairs the liver’s filtering function, allowing bacteria to pass from the bowel lumen to the bloodstream via the portal vein. Cirrhosis also is associated with a relative increase in aerobic gram-negative bacilli in the jejunum. A decrease in mucosal blood flow due to acute hypovolemia or drug-induced splanchnic vasoconstriction may compromise the intestinal barrier to enteric flora, thereby increasing the risk of bacteremia. Finally, bacterial translocation may occur with the movement of enteric organisms from the gut lumen through the mucosa to the intestinal lymphatics. From there bacteria can travel through the lymphatic system and enter the bloodstream via the thoracic duct. It is assumed that SBP caused by non-enteric organisms is also due to bacteremia secondary to another site of infection, with subsequent seeding of the peritoneum and ascitic fluid.
Resuscitation Physiology
Published in Kenneth D Boffard, Manual of Definitive Surgical Trauma Care: Incorporating Definitive Anaesthetic Trauma Care, 2019
The intestinal mucosa requires rapid synthesis of amino acids. Depletion of amino acids results in atrophy of the mucosa causing failure of the mucosal barrier. This may lead to bacterial translocation from the gut to the portal system. The extent of bacterial translocation in trauma has not been defined.10 The presence of food in the gut lumen is a major stimulus for mucosal cell growth. Food intake is invariably interrupted after major trauma, and the supply of glutamine may be insufficient for mucosal cell growth. Early nutrition (within 24–48 hours), and early enteral rather than parenteral feeding may prevent or reduce these events.
An update on the pharmacological management of autoimmune hepatitis
Published in Expert Opinion on Pharmacotherapy, 2021
Yooyun Chung, Mussarat N Rahim, Jonathon J Graham, Yoh Zen, Michael A Heneghan
There are a plethora of therapeutic targets and experimental therapies in development, but all are in early phases of testing. Potential novel therapeutic options include cell therapies targeting B-cell modulation and expansion of intrahepatic Tregs. Interventions directed at altering gut microbiota and bacterial translocation also merit exploration. Therapies which target Treg pathways are favorable as restoration of immune regulation is the ultimate long-term goal, as opposed to immunosuppression which has long-term side effects. Certain therapies, including pre-implantation factor, anti-BAFF therapy, autologous Treg transfer, and low-dose IL-2 therapy are currently being evaluated in clinical trials, so these agents may be available in the next 5 years. Other drugs to consider as adjunctive therapy are those which decelerate disease progression to cirrhosis and modulate fibrosis.
Fungal lysozyme leverages the gut microbiota to curb DSS-induced colitis
Published in Gut Microbes, 2021
Ida Søgaard Larsen, Benjamin A. H. Jensen, Erica Bonazzi, Béatrice S. Y. Choi, Nanna Ny Kristensen, Esben Gjerløff Wedebye Schmidt, Annika Süenderhauf, Laurence Morin, Peter Bjarke Olsen, Lea Benedicte Skov Hansen, Torsten Schröder, Christian Sina, Benoît Chassaing, André Marette
Compared to obesity, gut health is further disrupted in IBD with clear genetic links to diminished HDP production.18,19 Bacterial translocation is well established in patients with IBD20,21 associating with reduced gut barrier function22 and a change in gut microbiota composition.23,24 Thus, obesity and IBD exhibit similar GI complications, although the links between the two phenotypes remain inadequately described.25 When the gut microbiota was evaluated by 16S rRNA gene amplicons, no similarities in microbiota composition changes within patients with obesity and IBD were reported.26 However, with more advanced network analysis, common regulation of specific enzymes involved in the phosphotransferase system or the nitrate reductase pathway has been identified between these patient groups27 supported by a change in bacterial co-abundances.28 Similarly, frameshift mutations in the pattern recognition receptor, nucleotide-binding oligomerization domain-containing protein 2 (NOD2), predispose for human IBD,29 while genetic ablation of the same protein promotes IR in HFD-fed mice.30 Patients with IBD exhibit increased prevalence of IR and nonalcoholic fatty liver disease (NAFLD), thus supporting a close connection between the mentioned diseases.31,32 Still, IR and IBD are rarely studied together, although both pathologies are increasing worldwide.33,34
Mechanisms and consequences of gut commensal translocation in chronic diseases
Published in Gut Microbes, 2020
Rebecca L. Fine, Silvio Manfredo Vieira, Michael S. Gilmore, Martin A. Kriegel
Besides PPIs and NSAIDs, treatment with antibiotics can enable bacterial translocation.42 Antibiotic-treated mice are more susceptible to DSS-induced epithelial injury, translocation of live bacteria, and inflammasome-mediated damage.43 In addition to eradicating beneficial bacteria that contribute to barrier integrity, antibiotic use can lead to overgrowth of pathogenic bacteria. Ampicillin treatment, for example, promotes colonization with vancomycin-resistant Enterococcus (VRE) in mice and humans prior to bloodstream infections.44 Metronidazole and streptomycin treatment enable E. faecalis overgrowth and approximation to the epithelial border, where it can be visualized inside intestinal epithelial cells, deeper in the lamina propria and beyond the mucosa.45 Similarly, a 2-day course of ceftriaxone enabled E. faecalis and Lactobacillus spp. overgrowth and systemic dissemination to the liver, spleen, and MLN within 3–4 days of exposure, with subsequent clearance by 14 days. Of note, exposure to ceftriaxone did not affect TJ protein expression, fecal albumin, or permeability to FITC-dextran.46 Oral antibiotics were shown to induce colonic goblet cell-associated antigen passages that enabled translocation of live bacteria to MLN, which continued for ~5 days after antibiotic withdrawal.47 Thus, antibiotics may disrupt colonization resistance and physiological homeostatic processes, allowing for transient dissemination of bacteria even without overt intestinal pathology.