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The Gut and Heart Connection
Published in Mark C Houston, The Truth About Heart Disease, 2023
Alterations in the gut or intestinal barrier or lining (called the “enterocytes”) lead to dysfunction and increased intestinal leakage Certain types of bacteria called gram-negative bacteria may enter the blood to produce severe inflammation and damage to the arteries. The medical term for this is endotoxemia (internal toxins), which means that the bacteria, the components of the bacteria, the types of food that we eat, and the health of the gut may allow toxins to enter the blood and cause arterial damage. The chronic dietary intake of long-chain saturated fatty acids (SFAs) with refined carbohydrates and starches increases the gram-negative bacterial concentration by 70%. On the other hand, a vegetable intake, fiber, and probiotics decrease gram-negative gut concentration.
The Role of the Gut Microbiome in Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Dietary Interventions to Decrease Endotoxemia Include: Increase whole plant food.Increase low-mercury fish consumption.Avoid sugar and processed foods.Incorporate intermittent fasting.Increase dietary fiber and prebiotic consumption (especially foods high in oligofructose, inulin, and galactooligosaccharide).Soluble fibers are digested by enzymes into SCFAs.SCFAs constitute approximately 5%–10% of the energy source in healthy people.Fiber-enriched diets improve insulin sensitivity58 in lean and obese diabetic subjects.
Bacteria
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Infection with Gram-negative bacteria may result in endotoxemia. Antibodies to endotoxins will precipitate them in vitro but do not neutralize their toxicity. The enzymes released by the complement system following its activation effectively degrade endotoxins.
Circulating microbiome in patients with portal hypertension
Published in Gut Microbes, 2022
Rolandas Gedgaudas, Jasmohan S Bajaj, Jurgita Skieceviciene, Greta Varkalaite, Gabija Jurkeviciute, Sigita Gelman, Irena Valantiene, Romanas Zykus, Andrius Pranculis, Corinna Bang, Andre Franke, Christoph Schramm, Juozas Kupcinskas
Due to the presence of shunts that develop with liver cirrhosis, blood from mesenteric veins directly enters the systemic circulation, avoiding the liver barrier.1 Furthermore, endotoxins in healthy individuals are cleared from portal blood by Kupffer cells; however, liver injury that occurs in cirrhosis results in leakage and higher endotoxin levels in the hepatic and peripheral circulations.7 Endotoxemia, with or without viable bacterial translocation, is a common event in cirrhosis.19 Several studies have reported altered endotoxin levels in the portal circulation versus those in the peripheral circulation, indicating a potential intestinal origin for these bacterial products.7 Different levels of inflammatory cytokines have also been shown in systemic, portal, and hepatic circulation.7,20 A small recent study by Schierwagen et al.21 reported distinct microbiome compositions in different blood compartments of patients with cirrhosis; however, further data regarding this are needed. Analysis of the circulating microbiome in different blood compartments in patients with liver cirrhosis is important for several reasons. First, it is important to determine whether the severity of disease is linked to the reduced ability of the liver to clear microbes in hepatic blood outflow. Second, it is important to understand if the degree of PH is associated with circulating microbiome alterations as higher levels of PH may lead to increased microbial burden in the peripheral circulation due to shunting and increased gut permeability.21
An update on endotoxin neutralization strategies in Gram-negative bacterial infections
Published in Expert Review of Anti-infective Therapy, 2021
Klaus Brandenburg, Andra B Schromm, Günther Weindl, Lena Heinbockel, Wilmar Correa, Karl Mauss, Guillermo Martinez de Tejada, Patrick Garidel
Large animals such as sheep, pigs, or primates reproduce more accurately the pathophysiology of human sepsis but research with these species is expensive and entails very strict ethical regulations. Most experts agree on the need to use several models of different species (including non-rodents) during the preclinical evaluation of new therapies to avoid failures in subsequent clinical stages. Notably, several models involving experimental human endotoxemia are being developed in the last decades. In these models, human subjects are challenged with low amounts of purified LPS [71]. Whereas, these human models can be highly standardized and use a selected homogenous population, direct comparisons between experimental endotoxemia and clinical causes of systemic inflammation should always be made with caution.
2,4,6-Trihydroxy-3-geranyl acetophenone suppresses vascular leakage and leukocyte infiltration in lipopolysaccharide-induced endotoxemic mice
Published in Pharmaceutical Biology, 2021
Yee Han Chan, Nazmi Firdaus Musa, Yi Joong Chong, Siti Arfah Saat, Faizul Hafiz, Khozirah Shaari, Daud Ahmad Israf, Chau Ling Tham
Endotoxemia is a condition in which an endotoxin, primarily lipopolysaccharide (LPS), is present in the bloodstream due to bacterial infection (bacteraemia). This pathological event is known as 'blood poisoning,' which is deleterious to the host, as the endotoxin can be carried throughout the body and provoke hyperinflammatory responses that will eventually lead to sepsis (van Poelgeest et al. 2018). LPS is an outer membrane component of Gram-negative bacteria that binds to a Toll-like receptor 4 (TLR4) to trigger systemic inflammation and sepsis progression (Li et al. 2017). When LPS is engaged locally or systemically in high concentrations, it activates TLR4 and triggers a series of signalling pathways, which then leads to impaired vascular integrity and endothelial hyperpermeability as a result of a compromised junctional complex. Notably, once an inflammatory response is initiated, the activated signalling pathways will provoke the upregulation of various proinflammatory mediators, such as nuclear factor-kappa B (NF-κB), mitogen-activated protein kinases (MAPKs), and cytokines and chemokines, further exacerbating vascular leakage in an unrestricted manner (Li et al. 2017). These pathological conditions will lead to multiple organ failure and septic shock, eventually causing death (Polat et al. 2017).