Lipopolysaccharide (LPS)

Overview

Lipopolysaccharide (LPS), also known as endotoxin, is a fundamental component of the outer membrane of Gram-negative bacteria. ^[1] It is a large molecule that is part lipid and part polysaccharide, that forms a protective outer shield for the bacterium and serves as a potent trigger of the host’s immune response. In essence, LPS is the signature glycolipid of Gram-negative bacteria, crucial for their structural integrity and notable for its ability to stimulate strong innate immune reactions. Clinically, LPS is infamous as the endotoxin responsible for fever and shock in severe Gram-negative infections. Even minute quantities can induce fever (it is a potent pyrogen) and, if large amounts enter the bloodstream, a cascade of inflammation may lead to septic shock with multi-organ failure.^[2]

Role of LPS in Gram-Negative Bacterial Physiology

As a defining feature of the outer membrane in Gram-negative bacteria, lipopolysaccharide (LPS) is densely arranged in the outer leaflet, forming a rigid, protective layer that performs multiple essential functions. It serves as a molecular “brick-and-mortar” wall that fortifies membrane integrity, restricts the entry of harmful agents, and shields the bacterium from host immune responses. The lipid A and core oligosaccharide components form a hydrophobic and electrostatic barrier, while the variable O-antigen extends outward to obstruct complement deposition and immune recognition. In addition to its defensive roles, LPS contributes to bacterial adherence and biofilm development, facilitating colonization and environmental adaptation. Though some exceptional strains (e.g., Neisseria, Moraxella) can survive with modified outer membranes, most Gram-negative bacteria rely on LPS for viability.^[3] Thus, LPS is not merely a structural component but a multifunctional determinant of survival, virulence, and immune evasion.

Function	Mechanism / Significance
Structural Integrity	LPS reinforces the outer membrane’s architecture. Lipid A–core regions provide mechanical strength; mutants lacking lipid A are typically non-viable.
Permeability Barrier	The dense packing of lipid A acyl chains and cross-linked sugars restricts penetration of bile salts, detergents, and many antibiotics.
Immune Evasion	Long O-antigen chains sterically hinder complement deposition and antibody access, conferring resistance to opsonization and lysis.
Surface Attachment and Biofilms	Polysaccharide chains mediate adhesion to host tissues and surfaces. LPS-containing outer membrane vesicles promote biofilm formation and bacterial signaling.
Environmental Adaptability	Structural variability, especially in the O-antigen, allows bacteria to evade host immune recognition and adapt to specific niches or hosts.

1.
Adapted from Caroff M, Novikov A. Lipopolysaccharides: structure, function and bacterial identification. OCL. 2020;27:31-31.‌ ^[4]

Immunological Significance of Lipopolysaccharide (LPS)

From the perspective of the host’s immune system, lipopolysaccharide (LPS) is a prominent red flag indicating a Gram-negative bacterial invasion. It is one of the quintessential pathogen-associated molecular patterns (PAMPs) recognized by the innate immune system. When Gram-negative bacteria infect a host or LPS enters the body (for instance, through a breached gut barrier or an infection focus), the immune system rapidly detects it.

What is the immunological significance of LPS?

Immunological Process	Description and Significance

TLR4 Recognition

LPS, specifically its lipid A moiety, binds to Toll-like receptor 4 (TLR4) on immune cells with the help of MD-2 and CD14. This initiates a signaling cascade activating NF-κB and other transcription factors, leading to transcription of pro-inflammatory cytokine genes. LPS effectively functions as an innate immune alarm signal.

Cytokine Storm Trigger

Activation of immune cells by LPS leads to rapid secretion of inflammatory cytokines (e.g., TNF-α, IL-1, IL-6) and lipid mediators (e.g., prostaglandins). These mediators induce fever, increase vascular permeability, and recruit leukocytes. Even low doses of LPS can provoke robust inflammatory responses.

Balance of Responses

Low levels of LPS exposure (e.g., from commensals) may promote immune tolerance or priming, while high systemic levels (e.g., from infection or gut translocation) can trigger excessive cytokine release, leading to tissue injury, hypotension, and multi-organ dysfunction – the clinical picture of endotoxin shock.

Adapted from Caroff M, Novikov A. Lipopolysaccharides: structure, function and bacterial identification. OCL. 2020;27:31-31.‌ ^[5]

Conditions Associated with Elevated LPS

Elevated levels of lipopolysaccharide (LPS) in circulation, a state known as endotoxemia, are clinically significant because LPS is a potent trigger of inflammation via Toll-like receptor-4 (TLR4) on immune cells.^[6] While acute, high-grade endotoxemia (as in Gram-negative sepsis) can induce a cytokine storm and septic shock, even chronic low-grade elevations of LPS (“metabolic endotoxemia”) provoke persistent systemic inflammation. This sustained inflammatory tone is implicated in the pathogenesis of numerous chronic conditions, linking gut microbial dynamics to metabolic and cardiovascular disease.^[7][8] Below are key clinical conditions hallmarked by elevated LPS levels, with a brief explanation of the mechanistic or clinical significance in each case:

Condition	Mechanistic/Clinical Association with Elevated LPS
Gram-negative Sepsis (Septic Shock)	Severe Gram-negative bacterial infections release large amounts of LPS into the bloodstream, triggering an overwhelming TLR4-mediated cytokine cascade (cytokine storm). Endotoxin levels are extremely high in septic shock patients, who often develop multi-organ failure (acute kidney injury, hepatic dysfunction, coagulopathy) as a result. ^[9] “Endotoxic” septic shock is thus directly driven by LPS.
Obesity & Metabolic Syndrome	High-fat diets can induce a 2–3 fold rise in plasma LPS – a phenomenon termed metabolic endotoxemia – which in turn promotes chronic low-grade inflammation and insulin resistance.^[10][11] Obese individuals often exhibit increased gut permeability, enabling LPS translocation from the gut into circulation. The resulting endotoxemia is thought to initiate adipose tissue inflammation and metabolic disturbances characteristic of obesity and metabolic syndrome.
Type 2 Diabetes Mellitus (T2DM)	Persistent low-grade endotoxemia is a feature of T2DM and a driver of its inflammatory complications. Chronically elevated LPS activates innate immune cells, impairing insulin signaling. Prospective studies have shown that higher baseline endotoxin is associated with increased risk of developing T2DM.^[12][13] Thus, endotoxemia-linked inflammation contributes to the insulin resistance and beta-cell stress in diabetes.
Non-Alcoholic Fatty Liver Disease (NAFLD/NASH)	Gut-derived endotoxin plays a key role in the liver inflammation seen in NAFLD and its progression to steatohepatitis (NASH). Patients with NAFLD show higher circulating LPS and pro-inflammatory cytokines, indicating that endotoxemia drives hepatic Kupffer cell activation and fibrogenesis. Intestinal barrier dysfunction in NAFLD allows LPS to enter portal circulation, exacerbating liver injury and inflammation.^[14]
Atherosclerosis & Cardiovascular Disease	Chronic low-grade endotoxemia is implicated in atherosclerosis and heart disease by promoting endothelial inflammation and foam cell formation. Elevated LPS has been correlated with increased cardiovascular risk (e.g. higher C-reactive protein and incidence of events) in population studies. Notably, endotoxemia is considered a molecular link between distant infections (such as periodontal disease) and cardiometabolic disorders.^[15] In essence, circulating LPS contributes to the inflammatory milieu that accelerates atherogenesis.
Chronic Kidney Disease (CKD)	CKD patients experience “uremic” endotoxemia due to a combination of gut dysbiosis, impaired immune clearance, and intestinal barrier defects. Even at early stages, CKD is associated with significantly elevated plasma LPS levels. ^[16] This endotoxin burden drives systemic inflammation and malnutrition in CKD and is linked to vascular complications. Dialysis patients in particular have repetitive exposure to endotoxin (e.g. translocation during hemodialysis), which may contribute to chronic inflammation and cardiovascular mortality in CKD.
Alzheimer’s Disease	Neurodegenerative disorders such as Alzheimer’s dementia (AD) have been linked to peripheral endotoxemia. AD patients often exhibit higher serum LPS levels and an enhanced immune response to LPS, suggesting chronic exposure to endotoxin (for example, from periodontal or gut microbes) may trigger neuroinflammation. ^[17] LPS can activate microglia in the brain, and repeated low-dose endotoxemia is hypothesized to accelerate neurodegenerative pathology. Recent studies have found that chronic periodontitis and the associated endotoxin load precede and possibly promote AD development.^[18]

*(Note: Additional conditions like rheumatoid arthritis, endometriosis, depression, and HIV infection have also been associated with elevated LPS, but the above represent key examples.)*

Interventions That Reduce LPS

Mitigating endotoxemia has become a therapeutic target to reduce inflammation in metabolic and inflammatory diseases. Approaches to lower systemic or compartmentalized LPS levels focus on either preventing LPS generation/absorption at its source or neutralizing its effects downstream. Notably, diet and microbiome-directed interventions can strengthen the intestinal barrier and alter gut flora to produce less endotoxin.^[19] For example, increasing dietary fiber and polyphenols favor beneficial microbes and improve tight junction integrity, thereby reducing LPS translocation from the gut. In parallel, pharmacological strategies (including certain antibiotics and experimental agents) aim to directly decrease LPS-producing bacteria or bind and detoxify LPS. Anti-endotoxin therapies such as polymyxin B which binds the lipid A portion of LPS, or antibodies against LPS O-antigen have shown the ability to neutralize endotoxin in preclinical models.^[20] Below is a summary of interventions with evidence for reducing LPS levels or activity, from human trials or robust preclinical studies:

Intervention	Mechanism and Effect on LPS Levels
Apigenin	Apigenin is a dietary flavonoid (abundant in chamomile, parsley, etc.) with gut-targeted anti-inflammatory effects. It beneficially modulates the gut microbiota and fortifies the intestinal barrier, thereby reducing LPS absorption. In high-fat diet models of obesity, apigenin supplementation markedly lowered systemic LPS levels and associated low-grade inflammation. ^[21]
Orange Juice	Polyphenol- and vitamin C-rich orange juice has been shown to blunt postprandial endotoxemia. In a human clinical study, co-ingesting orange juice with a high-fat, high-carbohydrate meal prevented the usual meal-induced rise in plasma endotoxin and Toll-like receptor (TLR4) expression on immune cells. ^[22] Subjects who drank water or glucose with the same meal had significant increases in LPS, whereas orange juice abolished this LPS spike and the accompanying inflammatory oxidative stress response. This effect is attributed to citrus flavonoids (like hesperidin and naringenin) that improve gut barrier function and have direct LPS-neutralizing or anti-inflammatory properties.
Probiotics	Supplementing beneficial bacteria can reduce endotoxemia by competing with LPS-producing Gram-negative flora and enhancing mucosal barrier integrity. For instance, a 30-day trial of an oral spore-based probiotic (containing Bacillus species) in healthy adults significantly reduced the incidence of dietary endotoxemia, as fewer subjects showed LPS elevation after a fatty meal compared to placebo.^[23] This suggests improved gut barrier function (lower permeability) and altered microbiota. Likewise, traditional probiotics (e.g. Lactobacillus, Bifidobacterium strains) have demonstrated reductions in circulating LPS and inflammatory markers in conditions like metabolic syndrome.^[24] Overall, probiotics help sequester or degrade luminal LPS and tighten junctions, thus lowering systemic endotoxin exposure.
Inulin	Prebiotic fibers such as inulin stimulate growth of LPS-suppressing commensals and increase production of short-chain fatty acids (SCFAs) that heal the gut lining. In a randomized controlled trial of women with T2DM, 8 weeks of daily inulin supplementation led to a 27.9% decrease in plasma LPS levels (compared to placebo), alongside significant reductions in inflammatory cytokines and insulin resistance. ^[25] The improved metabolic profile was attributed to inulin’s modulation of gut microbiota and reinforcement of tight junction proteins, which curtailed LPS translocation. This evidence underscores dietary fiber as a viable strategy to reduce endotoxemia and inflammation in humans.
Rifaximin	Rifaximin is a gut-specific antibiotic that targets Gram-positive and Gram-negative bacteria without systemic absorption. By reshaping the intestinal microbiota, rifaximin can lower the endogenous production of endotoxin. In patients with NASH (non-alcoholic steatohepatitis), 28 days of rifaximin therapy significantly reduced serum endotoxin levels (endotoxin activity dropped, P = 0.03) and also improved liver enzymes and inflammatory markers.^[26] Similarly, rifaximin has been used in cirrhosis and metabolic syndrome to alleviate endotoxemia and related inflammation.^[27] The mechanism involves decreasing LPS-producing gut bacteria and intestinal permeability. Notably, because rifaximin is non-systemic, it reduces LPS at its source (the gut) while minimizing systemic side effects.
Curcumin	Curcumin has demonstrated the ability to reduce LPS-mediated inflammation by strengthening the gut barrier and detoxifying endotoxin. In rodent models of diet-induced metabolic syndrome, curcumin supplementation increased intestinal alkaline phosphatase activity (which dephosphorylates and neutralizes LPS) and preserved tight junction structure, thereby preventing rises in plasma LPS. ^[28] Diabetic rats on a high-fat diet showed significantly elevated serum LPS and TNF-α, but curcumin treatment decreased both LPS and inflammatory cytokine levels back toward normal.^[29] These effects are linked to curcumin’s reshaping of the gut microbiota (enriching beneficial taxa) and its direct inhibition of LPS-induced signaling pathways in intestinal cells. Some preliminary human studies echo these findings, supporting curcumin as a therapeutic adjunct to reduce endotoxemia and inflammation in metabolic diseases.

FAQs

What is LPS and where does it come from?

Lipopolysaccharide (LPS) is a large glycolipid molecule found in the outer membrane of Gram-negative bacteria. It is released either during bacterial growth or cell lysis and acts as a potent endotoxin capable of triggering host immune responses via Toll-like receptor 4 (TLR4) activation.

What is metabolic endotoxemia?

Metabolic endotoxemia refers to a 2–3 fold increase in circulating LPS levels, typically due to increased gut permeability. Unlike septic endotoxemia, it induces low-grade, chronic inflammation and is implicated in obesity, type 2 diabetes, NAFLD, and cardiovascular disease.

How is LPS detected in research and clinical studies?

The Limulus Amebocyte Lysate (LAL) assay is most commonly used, but it has limitations including false positives due to β-glucans and lipoproteins. Alternative or complementary methods include LBP (LPS-binding protein) assays and endotoxin activity assays (EAA).

Research Feed

April 9, 2010

•

What was studied?

Researchers evaluated whether co-ingesting orange juice with a high-fat, high-carbohydrate (HFHC) meal can neutralize the meal’s proinflammatory and oxidative effects. The study specifically focused on post-meal plasma endotoxin (lipopolysaccharide, LPS) levels and Toll-like receptor (TLR2 and TLR4) expression on immune cells. In this clinical trial, various inflammatory and oxidative stress markers (e.g. reactive oxygen species, cytokine signaling proteins, TLRs, and endotoxin) were measured after an HFHC meal consumed with orange juice, versus with water or a glucose drink.

Who was studied?

The study involved 30 healthy, normal-weight adults (men and women, age 20–40, BMI 20–25) divided into three equal groups. Each group consumed a 900-kcal HFHC meal accompanied by one of three beverages: water, 75 g glucose (300 kcal), or an equivalent 300-kcal orange juice serving. Blood samples were collected fasting and at 1, 3, and 5 hours post-meal to assess metabolic and inflammatory responses.

Key Findings

Orange juice prevents TLR2/4 upregulation. Only the water- and glucose-drink groups showed significant postprandial increases in mononuclear cell TLR2 and TLR4 mRNA (peaking ~34–87% above baseline), whereas the orange juice (OJ) group had no significant change. Consistently, plasma endotoxin concentrations rose by ~60–70% within hours after the HFHC meal with water or glucose, but this endotoxemia surge was completely prevented when orange juice was co-ingested. Thus, OJ effectively blocked the gut-derived LPS–TLR inflammatory axis underpinning postprandial inflammation.

Orange juice also blunted oxidative stress. The HFHC meal led to a spike in reactive oxygen species (ROS) generation by leukocytes in the water and glucose groups, but co-ingestion of OJ significantly curbed this ROS burstajcn.nutrition.org. For example, at 1 hour post-meal, mononuclear cell ROS production increased by ~62–63% with water or glucose, versus only ~47% with OJajcn.nutrition.org. Likewise, neutrophil ROS rose markedly after the meal + water/glucose, but remained minimal with OJ. Furthermore, OJ abrogated the meal-induced rises in other inflammatory mediators: mononuclear NF-κB–related signals, MMP-9 (matrix metalloproteinase-9) expression and plasma levels, and intracellular MAPK p38 activation were all significantly elevated post-meal with water or glucose, yet virtually unchanged when OJ was included. In short, orange juice neutralized the HFHC meal’s pro-oxidative and proinflammatory impact, preventing increased endotoxin, TLR2/4, and downstream inflammatory signaling that were otherwise observed postprandially.

Clinical Implications

These findings have important clinical implications for metabolic and cardiovascular health. Repeated episodes of postprandial inflammation and metabolic endotoxemia (transient entry of gut bacterial LPS after meals) are thought to contribute to insulin resistance and atherosclerosis. By showing that a polyphenol-rich beverage like orange juice can buffer the inflammatory effects of a high-fat, high-carb meal, this study suggests a practical dietary strategy to mitigate meal-induced inflammatory stress. The orange juice prevented the LPS surge and TLR4 upregulation, thereby interrupting a key microbe-driven inflammatory pathway. Clinically, such an approach could reduce the cumulative burden of inflammation and oxidative stress after unhealthy meals, potentially lowering the risk of metabolic syndrome and cardiovascular events over time. In essence, dietary components can modulate host–microbial interactions: here, orange juice’s flavonoids (like hesperidin) likely counteracted gut-derived endotoxin effects, attenuating postprandial inflammatory responses.

This underscores the need to consider not just macronutrient content but also food combinations and bioactive nutrients that neutralize proinflammatory triggers in the diet. For clinicians, advising the inclusion of polyphenol-rich foods or beverages with indulgent meals might be a stepping stone toward blunting post-meal inflammation and improving metabolic health.

January 11, 2021

•

What was reviewed?

This review, authored by Mohammad and Thiemermann (2021), comprehensively examines the concept of metabolic endotoxemia, defined as a diet-induced increase in circulating lipopolysaccharide (LPS) levels, and its relationship with systemic inflammation and chronic disease. The paper synthesizes preclinical and clinical findings that connect high-fat diets (HFDs), increased gut permeability ("leaky gut"), translocation of LPS, and the activation of Toll-like receptor 4 (TLR4)-mediated inflammatory pathways to the pathogenesis of obesity, type 2 diabetes mellitus (T2DM), non-alcoholic fatty liver disease (NAFLD), and cardiovascular disease. Additionally, it evaluates both pharmacological and dietary interventions, including antimicrobial peptides (AMPs), micronutrient modulation, and microbiome-targeted strategies to mitigate metabolic endotoxemia.

Who was reviewed?

The review draws from a diverse body of literature, including murine models (e.g., TLR4-deficient, ApoE-deficient, and HFD-fed mice), human studies in obese and diabetic individuals, and clinical interventions assessing endotoxemia through LPS or LPS-binding protein (LBP) markers. Special focus is placed on studies employing controlled dietary exposures, AMP assays, knockout models, and microbiome analysis to characterize the drivers and downstream effects of metabolic endotoxemia.

What were the most important findings?

Metabolic endotoxemia results from the translocation of gut-derived lipopolysaccharide (LPS) into systemic circulation, primarily due to dietary disruption of the intestinal epithelial barrier. HFDs induce gut dysbiosis, deplete beneficial taxa such as Bifidobacterium and Eubacterium spp., and reduce tight junction proteins (e.g., occludin, claudins, and ZO-1), resulting in increased intestinal permeability. This "leaky gut" condition facilitates LPS entry into the bloodstream, triggering TLR4/MyD88-mediated signaling cascades and NF-κB activation, thereby promoting systemic low-grade inflammation.

Clinical studies show elevated LBP and LPS levels in individuals with T2DM, atherosclerosis, and NAFLD. These increases correlate with heightened expression of pro-inflammatory cytokines such as TNF-α and IL-6 in adipose tissue and liver, as well as with metabolic parameters like waist-to-hip ratio and serum triglycerides. From a microbiome perspective, endotoxemia is consistently associated with altered gut microbial composition—particularly a decreased Firmicutes-to-Bacteroidetes ratio—and overexpression of TLR2/TLR4 in the intestinal tract.

The review also highlights interventions targeting metabolic endotoxemia. Antimicrobial peptides, such as defensins and LL-37, exhibit both bactericidal and LPS-neutralizing effects. Synthetic AMPs (e.g., Peptide 19-2.5) show potential in attenuating LPS-driven inflammation in sepsis models. Dietary strategies, including prebiotics (inulin, FOS), probiotics (Bifidobacterium, Lactobacillus), and micronutrient supplementation (zinc, vitamin D), offer promising routes to restore tight junction integrity and reduce circulating LPS. However, limitations in endotoxemia detection—primarily due to the unreliability of the LAL assay—complicate conclusions about causality.

What are the greatest implications of this review?

This review reinforces metabolic endotoxemia as a mechanistic link between diet, gut dysbiosis, and chronic systemic inflammation. It establishes a conceptual foundation for LPS as a biomarker and driver of cardiometabolic disease and supports microbiome-targeted interventions—especially AMP-based and dietary approaches—as plausible therapeutic strategies. However, it also underscores the limitations of current LPS detection methods (e.g., LAL assay) and calls for more robust assays and interventional trials to establish causality. For microbiome researchers, the paper offers microbial targets (Bifidobacterium, Eubacterium) and mechanistic endpoints (tight junction proteins, NF-κB, MyD88) to validate microbiome signatures of endotoxemia and develop microbiome-targeted interventions MBTIs.

References

Biochemistry, Lipopolysaccharide.. Farhana A, Khan YS.. (April 17, 2023.)
Clinical Sepsis and Death in a Newborn Nursery Associated with Contaminated Parenteral Medications.. CDC.gov. (Brazil, 1996. Cdc.gov.)
Lipopolysaccharides: structure, function and bacterial identification.. 1. Caroff M, Novikov A.. (OCL. 2020;27:31-31.)
Lipopolysaccharides: structure, function and bacterial identification.. 1. Caroff M, Novikov A.. (OCL. 2020;27:31-31.)
Lipopolysaccharides: structure, function and bacterial identification.. 1. Caroff M, Novikov A.. (OCL. 2020;27:31-31.)
Role of Metabolic Endotoxemia in Systemic Inflammation and Potential Interventions.. Mohammad S and Thiemermann C.. (Front. Immunol. 11:594150. (2021))
Role of Metabolic Endotoxemia in Systemic Inflammation and Potential Interventions.. Mohammad S and Thiemermann C.. (Front. Immunol. 11:594150. (2021))
Role of Metabolic Endotoxemia in Systemic Inflammation and Potential Interventions.. Mohammad S and Thiemermann C.. (Front. Immunol. 11:594150. (2021))
The role of endotoxin in septic shock.. Kellum, J.A., Ronco, C.. (Crit Care 27, 400 (2023).)
Role of Metabolic Endotoxemia in Systemic Inflammation and Potential Interventions.. Mohammad S and Thiemermann C.. (Front. Immunol. 11:594150. (2021))
Role of Metabolic Endotoxemia in Systemic Inflammation and Potential Interventions.. Mohammad S and Thiemermann C.. (Front. Immunol. 11:594150. (2021))
Role of Metabolic Endotoxemia in Systemic Inflammation and Potential Interventions.. Mohammad S and Thiemermann C.. (Front. Immunol. 11:594150. (2021))
Role of Metabolic Endotoxemia in Systemic Inflammation and Potential Interventions.. Mohammad S and Thiemermann C.. (Front. Immunol. 11:594150. (2021))
Role of Metabolic Endotoxemia in Systemic Inflammation and Potential Interventions.. Mohammad S and Thiemermann C.. (Front. Immunol. 11:594150. (2021))
Periodontitis and cardiometabolic disorders: The role of lipopolysaccharide and endotoxemia.. Pussinen PJ, Kopra E, Pietiäinen M, Lehto M, Zaric S, Paju S, Salminen A.. (Periodontol 2000. 2022 Jun;89(1):19-40.)
Circulating endotoxemia: a novel factor in systemic inflammation and cardiovascular disease in chronic kidney disease.. McIntyre CW, Harrison LE, Eldehni MT, Jefferies HJ, Szeto CC, John SG, Sigrist MK, Burton JO, Hothi D, Korsheed S, Owen PJ, Lai KB, Li PK.. (Clin J Am Soc Nephrol. 2011 Jan;6(1):133-41.)
Stress induces endotoxemia and low-grade inflammation by increasing barrier permeability.. de Punder K and Pruimboom L. (Front. Immunol. 6:223. (2015))
Stress induces endotoxemia and low-grade inflammation by increasing barrier permeability.. de Punder K and Pruimboom L. (Front. Immunol. 6:223. (2015))
The role of endotoxin in septic shock.. Kellum, J.A., Ronco, C.. (Crit Care 27, 400 (2023).)
The role of endotoxin in septic shock.. Kellum, J.A., Ronco, C.. (Crit Care 27, 400 (2023).)
Apigenin Alleviates Obesity-Associated Metabolic Syndrome by Regulating the Composition of the Gut Microbiome.. Qiao Y, Zhang Z, Zhai Y, Yan X, Zhou W, Liu H, Guan L and Peng L. (Front. Microbiol. 12:805827. (2022))
Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and Toll-like receptor expression.. Ghanim H, Sia CL, Upadhyay M, Korzeniewski K, Viswanathan P, Abuaysheh S, Mohanty P, Dandona P.. (Am J Clin Nutr. 2010 Apr;91(4):940-9.)
Oral spore-based probiotic supplementation was associated with reduced incidence of post-prandial dietary endotoxin, triglycerides, and disease risk biomarkers.. McFarlin BK, Henning AL, Bowman EM, Gary MA, Carbajal KM.. (World Journal of Gastrointestinal Pathophysiology. 2017;8(3):117-117.)
Effect of Probiotic Supplementation on Intestinal Permeability in Overweight and Obesity: A Systematic Review of Randomized Controlled Trials and Animal Studies.. DiMattia Z, Damani JJ, Van Syoc E, Rogers CJ.. (Adv Nutr. 2024 Jan;15(1):100162.)
Inulin controls inflammation and metabolic endotoxemia in women with type 2 diabetes mellitus: a randomized-controlled clinical trial.. Dehghan P, Gargari BP, Jafar-Abadi MA, Aliasgharzadeh A.. (Int J Food Sci Nutr. 2014 Feb;65(1):117-23.)
Efficacy of rifaximin on circulating endotoxins and cytokines in patients with nonalcoholic fatty liver disease.. Gangarapu, Venkatanarayanaa; Ince, Ali Tüzüna; Baysal, Birola; Kayar, Yusufa; Kiliç, Ulkanb; Gök, Özlemb; Uysal, Ömerc; Şenturk, Hakana.. (European Journal of Gastroenterology & Hepatology 27(7):p 840-845, July 2015.)
Rifaximin: beyond the traditional antibiotic activity.. Calanni, F., Renzulli, C., Barbanti, M. et al.. (J Antibiot 67, 667–670 (2014).)
Improvement of intestinal barrier function, gut microbiota, and metabolic endotoxemia in type 2 diabetes rats by curcumin.. Huang J, Guan B, Lin L, Wang Y.. (Bioengineered. 2021 Dec;12(2):11947-11958.)
Improvement of intestinal barrier function, gut microbiota, and metabolic endotoxemia in type 2 diabetes rats by curcumin.. Huang J, Guan B, Lin L, Wang Y.. (Bioengineered. 2021 Dec;12(2):11947-11958.)

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Lipopolysaccharide (LPS)

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Overview

Role of LPS in Gram-Negative Bacterial Physiology

Immunological Significance of Lipopolysaccharide (LPS)

Conditions Associated with Elevated LPS

Interventions That Reduce LPS

FAQs

Research Feed

What was studied?

Who was studied?

Key Findings

Clinical Implications

What was reviewed?

Who was reviewed?

What were the most important findings?

What are the greatest implications of this review?

References

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Lipopolysaccharide (LPS)

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Forgot Password

Overview

Role of LPS in Gram-Negative Bacterial Physiology

Immunological Significance of Lipopolysaccharide (LPS)

Conditions Associated with Elevated LPS

Interventions That Reduce LPS

FAQs

Research Feed

What was studied?

Who was studied?

Key Findings

Clinical Implications

What was reviewed?

Who was reviewed?

What were the most important findings?

What are the greatest implications of this review?

References

What's on your mind?