Nanoplasmonic biosensor for rapid detection of multiple viral variants in human serum.

As viruses constantly change due to mutation, variants are expected to emerge demanding development of sensors capable of detecting multiple variants using one single sensor platform. Herein, we report the integration of a synthetic binder against SARS-CoV-2 with a nanoplasmonic-based sensing technology, which enables the successful detection of spike proteins of Alpha, Beta and Gamma variants of SARS CoV-2. The recognition event is achieved by specific nanostructured molecularly imprinted polymers (nanoMIPs), developed against a region of the receptor binding domain (RBD) of the SARS CoV-2 spike protein. The transduction is based on the principle of localized surface plasmon resonance (LSPR) associated with silver nanostructures. The nanoMIPs-functionalised LSPR sensor allows for the detection of all 3 protein variants with a limit of detection of 9.71 fM, 7.32 fM and 8.81 pM using wavelength shifts respectively for Alpha, Beta and Gamma spike protein variants. This can be achieved within 30 min from the sample collection, both from blood and using nasal swab, thus making this sensor suitable for rapid detection of COVID-19. Additionally, the turnaround time for sensor development and validation can be completed in less than 8 weeks, making it suitable for addressing future pandemic needs without the requirement for biological binding agents, which is one of the bottlenecks to the supply chain in diagnostic devices.

A Risk Assessment Framework for the Socioeconomic Impacts of Electricity Transmission Infrastructure Failure Due to Space Weather: An Application to the United Kingdom.

Space weather phenomena have been studied in detail in the peer-reviewed scientific literature. However, there has arguably been scant analysis of the potential socioeconomic impacts of space weather, despite a growing gray literature from different national studies, of varying degrees of methodological rigor. In this analysis, we therefore provide a general framework for assessing the potential socioeconomic impacts of critical infrastructure failure resulting from geomagnetic disturbances, applying it to the British high-voltage electricity transmission network. Socioeconomic analysis of this threat has hitherto failed to address the general geophysical risk, asset vulnerability, and the network structure of critical infrastructure systems. We overcome this by using a three-part method that includes (i) estimating the probability of intense magnetospheric substorms, (ii) exploring the vulnerability of electricity transmission assets to geomagnetically induced currents, and (iii) testing the socioeconomic impacts under different levels of space weather forecasting. This has required a multidisciplinary approach, providing a step toward the standardization of space weather risk assessment. We find that for a Carrington-sized 1-in-100-year event with no space weather forecasting capability, the gross domestic product loss to the United Kingdom could be as high as £15.9 billion, with this figure dropping to £2.9 billion based on current forecasting capability. However, with existing satellites nearing the end of their life, current forecasting capability will decrease in coming years. Therefore, if no further investment takes place, critical infrastructure will become more vulnerable to space weather. Additional investment could provide enhanced forecasting, reducing the economic loss for a Carrington-sized 1-in-100-year event to £0.9 billion.

Elevated lipogenesis and diminished cholesterol synthesis in patients with hepatitis C viral infection compared to healthy humans.

UNLABELLED: Hepatitis C virus (HCV) exerts a profound influence on host lipid metabolism. It has been suggested that the synthesis of both fatty acids (FA) and cholesterol is dysregulated in HCV but this has not been directly quantified in humans. The purpose of this study was to measure lipogenesis and cholesterol synthesis using stable isotopes in patients with HCV (n = 5) and healthy control (n = 9) subjects recruited from the University of Alberta hospital. Blood samples were taken at fasting (0 and 24 hours) and after meals over the day to mimic typical food consumption and postprandial metabolism. Isolation of free cholesterol (FC), cholesteryl ester (CE), and triglyceride (TG) from plasma and very low-density lipoproteins (VLDL) was used to measure FA and cholesterol synthesis using deuterium uptake and isotope ratio mass spectrometry. FA composition was analyzed by gas chromatography. VLDL-TG levels of polyunsaturated fatty acids (PUFA), including linoleic and linolenic acid, were lower in HCV compared to control (P < 0.05 for both). Fasting hepatic lipogenesis was significantly higher in HCV (2.80 ± 0.55%) compared to control (1.19 ± 0.27%; P = 0.03). Conversely, fasting whole-body synthesis of FC (HCV 1.64 ± 0.28% versus control 8.78 ± 1.59%) and CE (HCV 0.26 ± 0.08% versus control 1.92 ± 0.25%), as well as hepatic FC synthesis (HCV 1.68 ± 0.26% versus control 8.12 ± 0.77%) was lower in HCV (P < 0.001 for all). CONCLUSION: These data provide evidence that lipogenesis is elevated while cholesterol synthesis is impaired in HCV, supporting previous findings from cellular and animal models. Low PUFA levels combined with elevated lipogenesis suggests a role for dietary PUFA supplementation in HCV patients.

More than 50% of players sustained a time-loss injury (>1†day of lost training or playing time) during the 2012 Super Rugby Union Tournament: a prospective cohort study of 17,340 player-hours.

BACKGROUND: Professional Rugby Union is a contact sport with a high risk of injury. OBJECTIVE: To document the incidence and nature of time-loss injuries during the 2012 Super Rugby tournament. DESIGN: Prospective cohort study. SETTING: 2012 Super Rugby tournament (Australia, New Zealand, South Africa). PARTICIPANTS: 152 players from 5 South African teams. METHODS: Team physicians collected daily injury data through a secure, web-based electronic platform. Data included size of the squad, type of day, main player position, training or match injury, hours of play (training and matches), time of the match injury, mechanism of injury, main anatomical location of the injury, specific anatomical structure of the injury, the type of injury, the severity of the injury (days lost). RESULTS: The proportion (%) of players sustaining a time-loss injury during the tournament was 55%, and 25% of all players sustained >1 injury. The overall incidence rate (IR/1000 player-hours) of injuries was 9.2. The IR for matches (83.3) was significantly higher than for training (2.1) and the IR was similar for forwards and backs. Muscle/tendon (50%) and joint/ligament (32.7%) injuries accounted for >80% of injuries. Most injuries occurred in the lower (48.1%) and upper limb (25.6%). 42% of all injuries were moderate (27.5%) or severe (14.8%), and tackling (26.3%) and being tackled (23.1%) were the most common mechanisms of injury. The IR of injuries was unrelated to playing at home compared with away (locations ≥6 h time difference). CONCLUSIONS: 55% of all players were injured during the 4-month Super Rugby tournament (1.67 injuries/match). Most injuries occurred in the lower (knee, thigh) or upper limb (shoulder, clavicle). 42% of injuries were severe enough for players to not play for >1 week.

Molecularly Imprinted Polymer Nanoparticles Enable Rapid, Reliable, and Robust Point-of-Care Thermal Detection of SARS-CoV-2.

Rapid antigen tests are currently used for population screening of COVID-19. However, they lack sensitivity and utilize antibodies as receptors, which can only function in narrow temperature and pH ranges. Consequently, molecularly imprinted polymer nanoparticles (nanoMIPs) are synthetized with a fast (2 h) and scalable process using merely a tiny SARS-CoV-2 fragment (∼10 amino acids). The nanoMIPs rival the affinity of SARS-CoV-2 antibodies under standard testing conditions and surpass them at elevated temperatures or in acidic media. Therefore, nanoMIP sensors possess clear advantages over antibody-based assays as they can function in various challenging media. A thermal assay is developed with nanoMIPs electrografted onto screen-printed electrodes to accurately quantify SARS-CoV-2 antigens. Heat transfer-based measurements demonstrate superior detection limits compared to commercial rapid antigen tests and most antigen tests from the literature for both the alpha (∼9.9 fg mL-1) and delta (∼6.1 fg mL-1) variants of the spike protein. A prototype assay is developed, which can rapidly (∼15 min) validate clinical patient samples with excellent sensitivity and specificity. The straightforward epitope imprinting method and high robustness of nanoMIPs produce a SARS-CoV-2 sensor with significant commercial potential for population screening, in addition to the possibility of measurements in diagnostically challenging environments.

Cholesterol ester and free fatty acids are modulated by policosanol in CaCo-2 intestinal cells.

OBJECTIVE: To investigate policosanol absorption by brush border membrane (BBM), metabolism in CaCo-2 enterocytes, and transport of policosanol metabolites across the basolateral membrane (BLM). It was hypothesized that policosanol is partially oxidized into fatty acids and then is incorporated into other lipids. METHODS: Policosanol was emulsified with phosphatidylcholine in the culture medium. The viability of cells was assessed via an MTT (3-[4,5]dimethylthiazol-2-yl-2,5-diphenyltetrazolim) assay. Control cells received only the same amount of "vehicle" (phosphatidylcholine) without policosanol. CaCo-2 cell monolayer and medium were collected; lipid was extracted and analyzed by thin-layer chromatography (TLC) and gas liquid chromatography (GLC). RESULTS: Eighty-six percent of policosanol added to the cell culture medium was absorbed after 48 hours' incubation. The amount of cholesterol ester fatty acid was significantly increased both in the cells and in the basolateral medium, and was reduced in the apical medium. Policosanol increased the quantity of free fatty acids in the basolateral medium and reduced the free fatty acid content of CaCo-2 cells. Further evaluation of lipid profiles indicated that policosanol modulated the fatty acid profile of cholesterol ester in the basolateral medium. CONCLUSION: It was concluded that policosanol or policosanol metabolites may modulate lipid metabolism and/or transport following absorption by the BBM, partial oxidation by the intestinal epithelium, and transport of policosanol metabolites across the BLM.

Ganglioside Alters Phospholipase Trafficking, Inhibits NF-κB Assembly, and Protects Tight Junction Integrity.

Background and Aims: Dietary gangliosides are present in human milk and consumed in low amounts from organ meats. Clinical and animal studies indicate that dietary gangliosides attenuate signaling processes that are a hallmark of inflammatory bowel disease (IBD). Gangliosides decrease pro-inflammatory markers, improve intestinal permeability, and reduce symptoms characteristic in patients with IBD. The objective of this study was to examine mechanisms by which dietary gangliosides exert beneficial effects on intestinal health. Methods: Studies were conducted in vitro using CaCo-2 intestinal epithelial cells. Gangliosides were extracted from milk powder and incubated with differentiated CaCo-2 cells after exposure to pro-inflammatory stimuli. Gut barrier integrity was assessed by electron microscopy, epithelial barrier function was examined by measuring transepithelial electric resistance, and content of HBD-2, IL-23, NF-κB, and sPLA2 was assessed by ELISA. Results: Ganglioside attenuated the decrease in integrity of tight junctions induced by pro-inflammatory stimuli and improved epithelial barrier function (P < 0.05). Ganglioside decreased the basolateral secretion of sPLA2 (P ≤ 0.05), lowered HBD-2 and IL-23 levels (P ≤ 0.05), and inhibited NF-κB activation (P ≤ 0.05). Conclusions: In summary, the present study indicates that ganglioside GD3 improves intestinal integrity by altering sPLA2 trafficking, and the production of pro-inflammatory mediators is mitigated by decreasing assembly of the NF-κB complex. Dietary gangliosides may have promising potential beneficial effects in IBD as decreased inflammatory signaling, improved intestinal integrity, and maintenance of epithelial barrier function have been demonstrated in vitro.

Immobilization of Molecularly Imprinted Polymer Nanoparticles onto Surfaces Using Different Strategies: Evaluating the Influence of the Functionalized Interface on the Performance of a Thermal Assay for the Detection of the Cardiac Biomarker Troponin I.

We demonstrate that a novel functionalized interface, where molecularly imprinted polymer nanoparticles (nanoMIPs) are attached to screen-printed graphite electrodes (SPEs), can be utilized for the thermal detection of the cardiac biomarker troponin I (cTnI). The ultrasensitive detection of the unique protein cTnI can be utilized for the early diagnosis of myocardial infraction (i.e., heart attacks), resulting in considerably lower patient mortality and morbidity. Our developed platform presents an innovative route to develop accurate, low-cost, and disposable sensors for the diagnosis of cardiovascular diseases, specifically myocardial infraction. A reproducible and advantageous solid-phase approach was utilized to synthesize high-affinity nanoMIPs (average size = 71 nm) for cTnI, which served as synthetic receptors in a thermal sensing platform. To assess the performance and commercial potential of the sensor platform, various approaches were used to immobilize nanoMIPs onto thermocouples or SPEs: dip coating, drop casting, and a covalent approach relying on electrografting with an organic coupling reaction. Characterization of the nanoMIP-functionalized surfaces was performed with electrochemical impedance spectroscopy, atomic force microscopy, and scanning electron microscopy. Measurements from an in-house designed thermal setup revealed that covalent functionalization of nanoMIPs onto SPEs led to the most reproducible sensing capabilities. The proof of application was provided by measuring buffered solutions spiked with cTnI, which demonstrated that through monitoring changes in heat transfer at the solid-liquid interface, we can measure concentrations as low as 10 pg L-1, resulting in the most sensitive test of this type. Furthermore, preliminary data are presented for a prototype platform, which can detect cTnI with shorter measurement times and smaller sample volumes. The excellent sensor performance, versatility of the nanoMIPs, and reproducible and low-cost nature of the SPEs demonstrate that this sensor platform technology has a clear commercial route with high potential to contribute to sustainable healthcare.

Protection of intestinal occludin tight junction protein by dietary gangliosides in lipopolysaccharide-induced acute inflammation.

OBJECTIVES: Intestinal permeability and barrier function are regulated by expression of tight junction proteins. Lipopolysaccharide (LPS), tumor necrosis factor-alpha, and interleukin-1beta induce expression of nitric oxide (NO) and reduce the expression of gut tight junction proteins. The purpose of this study was to determine whether dietary gangliosides (GGs) increase the concentration of the anti-inflammatory cytokine interleukin-10 (IL-10) in response to LPS, thereby inhibiting NO production and protecting gut occludin tight junction protein from degradation. MATERIALS AND METHODS: Rats were fed semipurified diets with (n = 16) or without (n = 16) GGs (0.1% w/w of total lipid). After 2 weeks of feeding, animals were injected with saline (n = 8/diet group) or LPS (n = 8/diet group) (IP, 3 mg mL(-1) kg(-1)). Intestinal tissue, mucosa, and blood sample were collected 6 hours post-LPS exposure. The effect of dietary GGs on production/expression of IL-10, NO, inducible NO synthase, and occludin protein was determined. RESULTS: Dietary GGs increased IL-10 content in intestinal mucosa significantly by 32-fold (P < 0.0001) and in plasma by 2.4-fold (P < 0.001). Feeding animals a ganglioside-enriched diet decreased total NO content in intestinal mucosa and plasma by 44% and 30%, respectively, and inhibited inducible NO synthase expression following LPS exposure compared with control animals. Dietary GGs reduced the degradation of occludin tight junction protein in response to LPS. CONCLUSIONS: Dietary GGs inhibit degradation of gut occludin tight junction protein during LPS-induced acute inflammation. Thus, dietary GGs have a role in protecting the integrity of the intestinal barrier during acute gut inflammation.

Uptake and fate of ganglioside GD3 in human intestinal Caco-2 cells.

Ganglioside GD3 is a glycosphingolipid found in colostrum, developing tissues, and tumors and is known to regulate cell growth, differentiation, apoptosis, and inflammation. Feeding a GD3-enriched diet to rats increases GD3 in intestinal lipid rafts and blood. The mechanism, efficiency, and fate of ganglioside absorption by human enterocytes have not been investigated. A model to study GD3 uptake by human intestinal cells was developed to test the hypothesis that enterocyte GD3 uptake is time and concentration dependent, with uptake efficiency and fate influenced by route of delivery. Caco-2 cells were exposed to GD3 on the apical or basolateral membrane (BLM) side for 6, 24, and 48 h. GD3 uptake, retention, transfer, and metabolism was determined. GD3 uptake across the apical and BLM was time and concentration dependent and reached a plateau. GD3 uptake across the BLM was more efficient than apical delivery. Apical GD3 was metabolized with some cell retention and transfer, whereas basolateral GD3 was mostly metabolized. This study demonstrates efficient GD3 uptake by enterocytes and suggests that the route of delivery influences ganglioside uptake and fate.

Dexamethasone and GLP-2 given to lactating rat dams influence glucose uptake in suckling and postweanling offspring.

BACKGROUND: Glucagon-like peptide-2 (GLP-2) enhances intestinal absorption in adult animals. Glucocorticosteroids accelerate the ontogeny of the intestine and increase sugar uptake in adult animals. Modifying the maternal diet during lactation alters nutrient uptake in the offspring. The authors hypothesized that GLP-2 and dexamethasone, when administrated to lactating rat dams, enhance sugar uptake in the suckling and postweanling offspring. METHODS: Rat dams were treated during lactation with GLP-2 (0.1 microg/g/day subcutaneously [SC], twice daily), dexamethasone (0.128 microg/g/day SC, once daily), GLP-2 + dexamethasone (same doses), or placebo. The suckling offspring were sacrificed at 19-21 days of age, and the postweanlings were sacrificed 4 weeks later. Intestinal glucose and fructose uptake was assessed using an in vitro ring technique. RESULTS: GLP-2 and dexamethasone resulted in lower body weights, and dexamethasone caused intestinal atrophy in sucklings. The jejunal atrophy in sucklings given dexamethasone was prevented by GLP-2 + dexamethasone. In sucklings, the maximal transport rate and the Michaelis affinity constant for ileal glucose uptake were both increased by GLP-2 and GLP-2 + dexamethasone. In contrast, in postweanlings, the maximal transport rate for jejunal glucose uptake was reduced by dexamethasone and GLP-2, as was ileal fructose uptake. CONCLUSIONS: Treating lactating rat dams with GLP-2 or dexamethasone enhances glucose uptake in sucklings, but the late effect is a reduction in glucose and fructose absorption in postweanlings. The nutritional significance of these findings remains to be established.

Loss of intestinal fatty acid binding protein increases the susceptibility of male mice to high fat diet-induced fatty liver.

Mice lacking I-FABP (encoded by the Fabp2 gene) exhibit a gender dimorphic response to a high fat/cholesterol diet challenge characterized by hepatomegaly in male I-FABP-deficient mice. In this study, we determined if this gender-specific modification of liver mass in mice lacking I-FABP is attributable to the high fat content of the diet alone and whether hepatic Fabp1 gene (encodes L-FABP) expression contributes to this difference. Wild-type and Fabp2-/- mice of both genders were fed a diet enriched with either polyunsaturated or saturated fatty acids (PUFA or SFA, respectively) in the absence of cholesterol. Male Fabp2-/- mice, but not female Fabp2-/- mice, exhibited increased liver mass and hepatic triacylglycerol (TG) deposition as compared to corresponding wild-type mice. In wild-type mice that were fed the standard chow diet, there was no difference in the concentration of hepatic L-FABP protein between males and females although the loss of I-FABP did cause a slight reduction of hepatic L-FABP abundance in both genders. The hepatic L-FABP mRNA abundance in both male and female wild-type and Fabp2-/- mice was higher in the PUFA-fed group than in the SFA-fed group, and was correlated with L-FABP protein abundance. No correlation between hepatic L-FABP protein abundance and hepatic TG concentration was found. The results obtained demonstrate that loss of I-FABP renders male mice sensitive to high fat diet-induced fatty liver, and this effect is independent of hepatic L-FABP.

Dexamethasone and GLP-2 administered to rat dams during pregnancy and lactation have late effects on intestinal sugar transport in their postweaning offspring.

Intestinal function in young animals is influenced by maternal factors, such as alterations in the maternal diet. Glucagon-like peptide 2 (GLP-2) enhances intestinal growth and absorption in mature animals. Glucocorticosteroids induce intestinal maturation in neonates and increase sugar uptake in adult animals. It is not known if maternally administered GLP-2 or glucocorticosteroids have persistent effects on intestinal transport in the offspring. This study was undertaken to determine (1) the influence of maternal GLP-2, dexamethasone (DEX) and GLP-2+DEX on intestinal sugar uptake in postweaning offspring and (2) if alterations in uptake are due to variations in intestinal morphology, sugar transporter abundance or the abundance of selected signals. Nursing rat dams were treated during pregnancy and lactation with GLP-2 (0.1 mug/g per day sc), DEX (0.128 microg/g per day sc), GLP-2+DEX or placebo. The offspring were sacrificed 4 weeks after weaning, and glucose and fructose uptake was determined using an in vitro intestinal ring uptake technique. sodium-dependent glucose transporter, glucose transporter (GLUT) 5, GLUT2, sodium potassium adenosine triphosphatase and selected signals were assessed by immunohistochemistry. The treatments did not affect body weights or intestinal morphology. GLP-2 and GLP-2+DEX increased jejunal fructose uptake, and GLP-2+DEX increased the jejunal and ileal maximal transport rate for glucose uptake. Protein kinase B and mammalian target of rapamycin abundance were also increased, while transporter abundance was unchanged. We speculate that these alterations in sugar uptake may be due to changes in the intrinsic activity of the transporters mediated by the phosphatidylinositol-3-kinase pathway. These alterations in uptake may have nutritional implications for the offspring of mothers who may be treated with GLP-2 or glucocorticosteroids.

Necrotizing enterocolitis: a multifactorial disease with no cure.

Necrotizing enterocolitis is an inflammatory bowel disease of neonates with significant morbidity and mortality in preterm infants. Due to the multifactorial nature of the disease and limitations in disease models, early diagnosis remains challenging and the pathogenesis elusive. Although preterm birth, hypoxic-ischemic events, formula feeding, and abnormal bacteria colonization are established risk factors, the role of genetics and vasoactive/inflammatory mediators is unclear. Consequently, treatments do not target the specific underlying disease processes and are symptomatic and surgically invasive. Breast-feeding is the most effective preventative measure. Recent advances in the prevention of necrotizing enterocolitis have focused on bioactive nutrients and trophic factors in human milk. Development of new disease models including the aspect of prematurity that consistently predisposes neonates to the disease with multiple risk factors will improve our understanding of the pathogenesis and lead to discovery of innovative therapeutics.

The Modifying Effects of Galactomannan from Canadian-Grown Fenugreek (Trigonella foenum-graecum L.) on the Glycemic and Lipidemic Status in Rats.

Using high sucrose-fed male Sprague-Dawley rats, a study was conducted to determine the effects of feeding Galactomannan (GAL), a soluble dietary fiber extracted from Canadian-grown fenugreek seeds, on blood lipid and glucose responses. Rats (n = 8, 175-200 g) were randomly assigned to one of three high sucrose diets containing 10% cellulose (control), 7.5% cellulose + 2.5% GAL, and 5% cellulose + 5% GAL, respectively for 4 weeks. After 3 weeks, an oral glucose tolerance test (OGTT) was performed on each rat. A week later blood samples were collected to determine the effect on blood lipids. A significant reduction in glycemic response was observed only in 5% GAL group at 120 min following OGTT, when compared with that of control and 2.5% GAL groups. The plasma level of insulin was also significantly reduced (p<0.001) in 5% GAL-fed rats but at all times during OGTT. These animals also showed a reduction in body weight gain (p<0.05) in parallel with less food intake (p<0.05). All GAL-fed (2.5% and 5.0%) rats had significantly reduced plasma levels of triglycerides and total cholesterol in association with a reduction in epididymal adipose weight. Overall, this study demonstrated that feeding GAL from Canadian-grown fenugreek seeds has the potential to alter glycemic and lipidemic status and reduce abdominal fat in normal rats.

Dietary ganglioside inhibits acute inflammatory signals in intestinal mucosa and blood induced by systemic inflammation of Escherichia coli lipopolysaccharide.

Our previous study demonstrated that feeding ganglioside increased total ganglioside content while decreasing cholesterol and caveolin-1 content in developing rat intestinal lipid microdomains. Cholesterol or caveolin depletion in membranes inhibits inflammatory signaling by disrupting microdomain structure. We hypothesized that dietary ganglioside-induced reduction in cholesterol content will reduce proinflammatory mediators in the intestinal mucosa after acute exposure to bacterial endotoxin. Weanling rats were fed semipurified diets with 0.1% (wt/wt of total fat) gangliosides (treatment) or without ganglioside (control). After 2 weeks of feeding, half of animals from each diet group were injected with saline or lipopolysaccharide (LPS) endotoxin (Escherichia coli serotype O111:B4, intraperitoneal, 3 mg/kg body weight) to induce acute gut inflammation. Intestinal mucosa and blood were collected after 6 h. The effect of dietary ganglioside on proinflammatory mediators including cholesterol, platelet-activating factor, prostaglandin E2, leukotriene B4 (LTB4), interleukin-1beta (IL-1beta), and tumor necrosis factor-alpha (TNF-alpha) was determined in inflamed mucosa and blood. Feeding animals the control diet increased cholesterol content in intestinal lipid microdomains by 92% after LPS injection compared with saline injection. Animals fed the ganglioside diet significantly decreased cholesterol content in lipid microdomains by 60% compared with animals fed the control diet. Feeding animals the ganglioside diet increased total ganglioside content by 90% while decreasing platelet-activating factor content by 45% in the inflamed mucosa by acute systemic exposure to LPS compared with animals fed the control diet. When animals were fed the ganglioside diet, the levels of prostaglandin E2, LTB4, IL-1beta, and TNF-alpha were lower in inflamed mucosa, and LTB4, IL-1beta, and TNF-alpha were decreased in plasma by 41%, 58%, and 55% compared with control animals, respectively. The present study demonstrates that dietary gangliosides inhibit proinflammatory signals in the intestine and blood induced by acute inflammation of LPS and suggests therapeutic potential in the treatment and management of acute local and systemic inflammatory diseases.