Browsing by Subject "LPS"
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(2016)Gastrointestinal symptoms such as diarrhea, cramping, nausea and gastric pain occur frequently in runners during training and competitions. The mechanisms leading to the distress are not fully understood, nor the reason why some remain asymptomatic. However, hyperthermia induced by exercise elevation of core temperature and oxidative damage due to reduced gastric blood flow have been postulated to affect the intestinal epithelial cells. Both sources of stress disrupt the binding of the epithelial tight junction proteins and increase permeability of the membrane to luminal endotoxins. Endotoxins reaching the blood stream through leaky tight junctions lead to an inflammatory response mediated by cytokines. These mechanisms may underlie the gastrointestinal symptoms often experienced by endurance athletes. The aim of this study was to measure running-induced changes in intestinal permeability and inflammatory markers and investigate their association with gastrointestinal symptoms. A secondary objective was to inspect possible correlations between gastrointestinal symptom occurrence and intake of certain nutrients. A total of 17 active runners were allocated into a control group (asymptomatic) or a symptomatic group based on a symptom history questionnaire and completed a 90-minute running test. Intestinal permeability at baseline and after the run were assessed via urine recovery of orally administered Iohexol . LPS (endotoxin) and zonulin concentrations were determined from serum samples. Participants kept a food diary for three days before each measurement and filled out a symptom questionnaire after the run. No significant difference was found in intestinal permeability between symptomatic and asymptomatic runners either at rest or following strenuous exercise. However, both groups experienced a significant increase in intestinal permeability from baseline to after running. LPS concentrations were significantly higher at baseline in the symptomatic group. This may explain the higher symptom occurrence in the symptomatic group. Zonulin levels were higher in control group than symptom group after the run. Zonulin concentration was also higher in the control group after the run compared to baseline. The symptom group reported more stomach pain and stool changes after running compared to controls. Comparison of average intake of various nutrients between the two groups showed no significant differences, indicating an individual predisposition as the cause of symptoms rather than diet alone. The lack of difference in intestinal permeability between the groups combined with the difference in symptom occurrence indicates that intestinal permeability changes alone do not account for symptom development. A possible factor may be individual differences in intestinal mucosa repair ability or some underlying pathology.
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(2016)Non-alcoholic fatty liver disease (NAFLD) is currently the most common liver disease in the western world. The human intestinal microbiota possesses enormous metabolic and immunomodulatory capabilities, and together with increased intestinal permeability, changes in the microbiota have been linked to the development of NAFLD. However, human studies so far have yielded contradictory findings regarding the compositional microbiota changes and provided little mechanistic understanding due to the predominance of cross-sectional studies. The aim of this study was to study human intestinal microbiota and gut permeability in NAFLD. Real-time PCR was employed to quantify the key intestinal bacterial groups in overweight or obese subjects with (n = 12) and without (n = 19) NAFLD, and in response to hypercaloric overfeeding, where participants were provided with three compositionally distinct diets to temporarily increase liver fat. In addition to the comparative analysis, the microbiota results were correlated to serum markers of intestinal permeability and metabolic endotoxemia, as well as clinical parameters related to NAFLD. The results show that host lipid metabolism and the gut microbiota, specifically Bacteroidetes and Clostridium cluster XIVa, are firmly intercorrelated. Bacteroidetes were found to be less abundant in subjects with NAFLD and correlate negatively with liver fat and serum triglycerides at baseline. Clostridium cluster XIVa, a dominant Firmicute group, was positively associated with serum triglycerides and pro-inflammatory markers but negatively with intestinal permeability. The relative abundance of Bacteroidetes as well as the markers of metabolic endotoxemia changed significantly in response to overfeeding, while no diet-induced systematic effects were found in Clostridium cluster XIVa, total bacteria, Escherichia coli group, Bifidobacterium or gut permeability. Our results based on a targeted microbiota analysis suggest that the role of the intestinal microbiota and gut permeability on triggering metabolic disarrangement and NAFLD in humans is inferior to other stimuli, such as diet.
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(2021)Tässä kirjallisuuskatsauksessa tarkastellaan lipopolysakkaridin (LPS) vaikutuksia immunologisiin parametreihin sekä vieroitetun porsaan immunologisia ja kehityksellisiä piirteitä, jonka vuoksi ne ovat alttiita sairastumaan tulehduksellisiin sairauksiin. Vieroitus tuotanto-olosuhteissa aiheuttaa porsaille stressiä ympäristön, ruokinnan ja sosiaalisten muutosten vuoksi. Porsaat ovat alttiita sairastumaan vieroituksen jälkeiseen ripuliin, sillä niiden immuunipuolustus ja suolisto ovat vielä kehittymässä vieroituksen aikaan. Vieroitusripulia aiheuttavia taudinaiheuttajia Suomessa ovat etenkin Escherichia coli, Brachyspira pilosicoli ja Lawsonia intracellularis, jotka ovat gram-negatiivisia bakteereja. Suolistotulehdukset aiheuttavat taloudellista haittaa sikataloudelle ja heikentävät eläinten hyvinvointia. Bakteeri-infektioiden hoidon seurauksena lisääntynyt antibioottien kulutus edistää antibioottiresistenssin kehittymistä. LPS on gram-negatiivisen bakteerin solukalvon ulompi osa, joka aktivoi voimakkaasti luontaista immuunipuolustusta. Lipopolysakkaridin seurauksena tulehdusta edistävien sytokiinien, kuten interleukiini-6:n, tuumorinekroositekijä alfan ja interleukiini-1 beetan pitoisuudet kohoavat nopeasti LPS-altistuksen jälkeen. Tämä johtaa akuutin vaiheen vasteen käynnistymiseen ja akuutin vaiheen proteiinien tuotantoon. Sian tärkeimmät akuutin vaiheen proteiinit ovat haptoglobiini, porcine major acute phase protein, C-reaktiivinen proteiini ja seerumin amyloidi A, joiden pitoisuutta voidaan mitata verestä tai syljestä. LPS vaikuttaa myös muiden immunologisten parametrien kuten adenosiinideaminaasin (ADA) pitoisuuteen. ADA:n pitoisuutta voidaan käyttää akuutin vaiheen proteiinien tapaan sairaiden eläinten tunnistamiseen sekä eläinten terveydentilan ja hyvinvoinnin arvioinnin tukena. Lisäksi LPS vaikuttaa kortisolin tuotantoon. Eri immunologisten parametrien vasteiden kestot LPS-altistuksen jälkeen voivat kuitenkin vaihdella.
Now showing items 1-3 of 3