Fecal Endotoxin Research Articles

Host genotype affects endotoxin release in excreta of broilers at slaughter age.

Host genotype, early post-hatch feeding, and pre- and probiotics are factors known to modulate the gut microbiome. However, there is a knowledge gap on the effect of both chicken genotype and these dietary strategies and their interplay on fecal microbiome composition and diversity, which, in turn, can affect the release of endotoxins in the excreta of broilers. Endotoxins are a major concern as they can be harmful to both animal and human health. The main goal of the current study was to investigate whether it was possible to modulate the fecal microbiome, thereby reducing endotoxin concentrations in the excreta of broiler chickens. An experiment was carried out with a 2 × 2 × 2 factorial arrangement including the following three factors: 1) genetic strain (fast-growing Ross 308 vs. slower growing Hubbard JA757); 2) no vs. combined use of probiotics and prebiotics in the diet and drinking water; and 3) early feeding at the hatchery vs. non-early feeding. A total of 624 Ross 308 and 624 Hubbard JA757 day-old male broiler chickens were included until d 37 and d 51 of age, respectively. Broilers (N = 26 chicks/pen) were housed in a total of 48 pens, and there were six replicate pens/treatment groups. Pooled cloacal swabs (N = 10 chickens/pen) for microbiome and endotoxin analyses were collected at a target body weight (BW) of 200g, 1kg, and 2.5kg. Endotoxin concentration significantly increased with age (p = 0.01). At a target BW of 2.5kg, Ross 308 chickens produced a considerably higher amount of endotoxins (Δ = 552.5EU/mL) than the Hubbard JA757 chickens (p < 0.01). A significant difference in the Shannon index was observed for the interaction between the use of prebiotics and probiotics, and host genotype (p = 0.02), where Ross 308 chickens with pre-/probiotics had lower diversity than Hubbard JA757 chickens with pre-/probiotics. Early feeding did not affect both the fecal microbiome and endotoxin release. Overall, the results suggest that the chicken genetic strain may be an important factor to take into account regarding fecal endotoxin release, although this needs to be further investigated under commercial conditions.

Regional venous\u2013arterial CO2 to arterial\u2013venous O2 content difference ratio in experimental circulatory shock and hypoxia

BackgroundVenous–arterial carbon dioxide (CO2) to arterial–venous oxygen (O2) content difference ratio (Cv-aCO2/Ca-vO2) > 1 is supposed to be both sensitive and specific for anaerobic metabolism. What regional hemodynamic and metabolic parameters determine the ratio has not been clarified.ObjectivesTo address determinants of systemic and renal, spleen, gut and liver Cv-aCO2/Ca-vO2.MethodsPost hoc analysis of original data from published experimental studies aimed to address effects of different fluid resuscitation strategies on oxygen transport, lactate metabolism and organ dysfunction in fecal peritonitis and endotoxin infusion, and from animals in cardiac tamponade or hypoxic hypoxia. Systemic and regional hemodynamics, blood flow, lactate uptake, carbon dioxide and oxygen-derived variables were determined. Generalized estimating equations (GEE) were fit to assess contributors to systemic and regional Cv-aCO2/Ca-vO2.ResultsMedian (range) of pooled systemic Cv-aCO2/Ca-vO2 in 64 pigs was 1.02 (0.02 to 3.84). While parameters reflecting regional lactate exchange were variably associated with the respective regional Cv-aCO2/Ca-vO2 ratios, only regional ratios were independently correlated with systemic ratio: renal Cv-aCO2 /Ca-vO2 (β = 0.148, 95% CI 0.062 to 0.234; p = 0.001), spleen Cv-aCO2/Ca-vO2 (β = 0.065, 95% CI 0.002 to 0.127; p = 0.042), gut Cv-aCO2/Ca-vO2 (β = 0.117, 95% CI 0.025 to 0.209; p = 0.013), liver Cv-aCO2/Ca-vO2 (β = − 0.159, 95% CI − 0.297 to − 0.022; p = 0.023), hepatosplanchnic Cv-aCO2/Ca-vO2 (β = 0.495, 95% CI 0.205 to 0.786; p = 0.001).ConclusionIn a mixed set of animals in different shock forms or during hypoxic injury, hepatosplanchnic Cv-aCO2/Ca-vO2 ratio had the strongest independent association with systemic Cv-aCO2/Ca-vO2, while no independent association was demonstrated for lactate or hemodynamic variables.

Effect of probiotics on the intestinal microbiota of hemodialysis patients: a randomized trial.

Intestinal dysbiosis contributes to the progression of renal failure and cardiovascular diseases in patients with chronic kidney disease. Probiotics is a promising intervention to improving intestinal dysbiosis. A double-blind clinical trial to investigate the ability of probiotics to modulate gut microbiota compositions in patients receiving hemodialysis (HD) was undertaken. Fifty HD patients were enrolled and randomized, receiving either probiotics or placebo for 6months. The responses to the interventions on gut microbiome, serum and fecal metabolome, serum albumin and endotoxin, endothelial activation markers and inflammatory markers were assessed. Totally, 22 in the probiotics group (11 males; 14 non-diabetic) and 23 in the placebo group (13 males; 17 non-diabetic) completed the study. Compared to that in the placebo group, probiotics did not significantly alter species diversity of the fecal microbiome. Probiotics did, however, restore the community composition, with particular significance in non-diabetic HD patients (P = 0.007 by Adonis analysis). Specifically, according to the results of linear discriminate analysis effect size, probiotics raised the proportions of family Bacteroidaceae and Enterococcaceae, and reduced Ruminococcaceae, Halomonadaceae, Peptostreptococcaceae, Clostridiales Family XIII. Incertae Sedis and Erysipelotrichaceae in non-diabetic HD patients. Additionally, probiotics reduced the abundances of several uremic retention solutes in serum or feces, including indole-3-acetic acid-O-glucuronide, 3-guanidinopropionic acid, and 1-methylinosine (P < 0.05). In the probiotic arm, no significant changes were observed in other secondary outcomes. Taken together, outcomes from this study suggest that probiotics do have benefits on improving intestinal imbalances and lowering exposure to several uremic toxins in HD patients.

370 Dietary soluble fiber increases the intestinal butyrate-producing bacteria, reduces intestinal permeability, and improves metabolic syndrome in sows during perinatal period

Abstract In humans, metabolic and immune changes during the perinatal period also describe metabolic syndrome. Gut microbiota can cause symptoms of metabolic syndrome in pregnant women. Gut microbiota modulations caused by pregnancy nutrition constitute an interesting target in the metabolic status of pregnant individual. However, studies investigating the changes of the metabolic characteristics and gut microbiota in sows throughout pregnancy and lactation are lacking, and the effects of soluble fiber diet during pregnancy on them are still underexplored. Sows were allocated to either control or 2.0% pregelatinized waxy maize starch plus guar gum (SF) dietary treatment during gestation. The metabolic characteristics, gut permeability and inflammation status, and gut microbiota composition and metabolism of sows during pregnancy and lactation were analysed. The plasma levels of hs-CRP and HOMA-IR values were increased in days 109 of gestation (G109) and days 3 of lactation (L3), while dietary SF reduced plasma hs-CRP concentrations and the HOMA-IR values. The levels of plasma zonulin and fecal endotoxin and lipocalin-2 were increased in G109 and L3, while dietary SF reduced elevation of plasma zonulin and endotoxin and fecal lipocalin-2. Next-generation sequencing analysis revealed that dietary SF increased levels of butyrate-producing Ruminococcaceae, Lachnospiraceae, and Oscillospira. The fecal and plasma levels of butyrate were also increased. Additionally, the increased relative abundances of Lachnospiraceae in SF sows negatively correlated with plasma hs-CRP and HOMA-IR while Oscillospira was negatively fecal lipocalin-2. Our data reveal that the sow exhibits a metabolic syndrome and dramatical changes in gut microbiota during perinatal period. Besides, dietary SF has beneficial effects on insulin sensitivity, intestinal permeability and inflammation maybe via increasing butyrate-producing bacteria and butyrate production.

PSIV-28 Effects of replacing zinc oxide and antibiotics with NeoPrime® on growth performance and plasma and fecal endotoxin concentration in nursery pigs.

PSIV-28 Effects of replacing zinc oxide and antibiotics with NeoPrime® on growth performance and plasma and fecal endotoxin concentration in nursery pigs.

Metabolic Syndrome During Perinatal Period in Sows and the Link With Gut Microbiota and Metabolites.

In humans, the metabolic and immune changes occurring during perinatal period also describe metabolic syndrome. Gut microbiota can cause symptoms of metabolic syndrome in pregnant women. Increased gut permeability is also involved in metabolic disorders in non-pregnant hosts. However, longitudinal studies investigating the changes in metabolic characteristics, gut microbiota, and gut permeability of sows throughout pregnancy and lactation are lacking. The correlation between gut microbiota and metabolic status of sows is also poorly known. The present study was conducted to investigate the temporal variations in sow metabolic characteristics, gut microbiota, gut permeability, and gut inflammation at days 30 (G30) and 109 (G109) of gestation and days 3 (L3) and 14 (L14) of lactation. Results showed that insulin sensitivity was decreased in L3. Circulating concentrations of pro-inflammatory cytokine IL-6 increased in G109 and L3. 16S rRNA gene sequencing of the V3-V4 region showed that gut microbiota changed dramatically across different reproductive stages. The bacterial abundance and alpha diversity in L3 were the lowest. The phyla Proteobacteria and Fusobacteria exhibited the highest relative abundance in L3. Among the genera, Bacteroides, Escherichia_Shigella, and Fusobacterium were highest, but Oscillospira the lowest, in relative abundance in L3. The fecal levels of acetate and total short-chain fatty acids were increased in G109, but fecal butyrate concentrations were markedly decreased in L3. The plasma zonulin concentrations, a biomarker for gut permeability, were increased in G109 and L3. The plasma endotoxin concentrations were increased in L3. Furthermore, levels of fecal lipocalin-2 and pro-inflammatory cytokines IL-6 and TNF-α were increased in G109 and L3. In contrast, fecal levels of anti-inflammatory cytokine IL-10 were significantly decreased in G109 and L3. Additionally, the increased relative abundances of Fusobacterium in L3 were positively correlated with plasma zonulin and fecal endotoxin but negatively correlated with fecal IL-10. These findings indicate that the mother sow exhibits a metabolic syndrome and dramatical changes in gut microbiota during perinatal period, especially in early lactation. Besides, increased gut permeability and plasma endotoxin concentrations caused by negative microbial changes would possibly be the potential mechanisms under which sow’s metabolic disorders and inflammatory status were exacerbated during early lactation.

Flos Lonicera Combined with Metformin Ameliorates Hepatosteatosis and Glucose Intolerance in Association with Gut Microbiota Modulation.

The gut microbiota is important in energy contribution, metabolism and immune modulation, and compositional disruption of the gut microbiota population is closely associated with chronic metabolic diseases like type 2 diabetes (T2D) and non-alcoholic fatty liver disease (NAFLD). Metformin (MET) and Flos Lonicera (FL) are common treatments for metabolic diseases in Western and Oriental medicinal fields. We evaluated the effect of treatment with FL and MET in combination on hepatosteatosis, glucose tolerance, and gut microbial composition. FL and MET were administered to Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an animal model of genetic T2D and NAFLD. The FL+MET treatment reduced liver weight, serum cholesterol, insulin resistance, and hepatic MDA level and modulated the gut microbial composition. More specifically, the genera of Prevotella and Lactobacillus were negatively associated with the body and liver weights, hepatic TG and TC content, and serum insulin level. However, the relative abundance of these genera decreased in response to the FL+MET treatment. Interestingly, pathway prediction data revealed that the FL+MET treatment attenuated lipopolysaccharide-related pathways, in keeping with the decrease in serum and fecal endotoxin levels. FL and MET in combination exerts a synergistic effect on the improvement of hepatosteatosis and insulin sensitivity in OLETF rats, and modulates gut microbiota in association with the effect.

Houttuynia cordata Facilitates Metformin on Ameliorating Insulin Resistance Associated with Gut Microbiota Alteration in OLETF Rats.

Metformin and Houttuynia cordata are representative anti-diabetic therapeutics in western and oriental medicine, respectively. The current study examined the synergistic anti-diabetic effect of Houttuynia cordata extraction (HCE) and metformin combination in Otsuka Long–Evans Tokushima Fatty (OLETF) rats. Fecal microbiota were analyzed by denaturing gradient gel electrophoresis (DGGE) and real-time PCR. Combining HCE + metformin resulted in significantly ameliorated glucose tolerance (oral glucose tolerance test (OGTT))—the same as metformin alone. Particularly, results of the insulin tolerance test (ITT) showed that combining HCE + metformin dramatically improved insulin sensitivity as compared to metformin treatment alone. Both fecal and serum endotoxin, as well as cytokines (tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6)) were significantly ameliorated by HCE + metformin compared to metformin alone. Meanwhile, the activation of AMPK (adenosine monophosphate-activated protein kinase) by metformin was distinctly enhanced by HCE. Both of HCE and metformin evidently changed the gut microbiota composition, causing the alteration of bacterial metabolite, like short-chain fatty acids. H. cordata, together with metformin, exerts intensive sensibilization to insulin; the corresponding mechanisms are associated with alleviation of endotoxemia via regulation of gut microbiota, particularly Roseburia, Akkermansia, and Gram-negative bacterium.

Determination of certain bacterial groups in gut microbiota and endotoxin levels in patients with nonalcoholic steatohepatitis.

In recent years, the role of the gut microbiota has emerged in several diseases. Herein we aimed to determine the fecal microbiota, endotoxin levels, and inflammation markers in patients with nonalcoholic steatohepatitis (NASH) and healthy controls. A total of 46 NASH patients and 38 healthy controls were included. NASH patients were diagnosed according to the steatosis, activity, and fibrosis score/fatty liver inhibition of progression algorithm. 16S rRNA gene-targeted specific primers were used for quantification of certain bacterial groups, and a plasmid library was constructed and sequenced in order to determine dominant Lactobacillus and Bifidobacterium members in patients and controls. Significantly decreased Akkermansia muciniphila and increased Enterobacteriaceae levels were determined in patients compared to healthy controls even after adjusting for the body mass index (BMI) and age. Patients with ≥F2 fibrosis had significantly higher Enterobacteriaceae levels compared to F0-F1 fibrosis. Serum endotoxin and high-sensitivity C-reactive protein levels were significantly higher in patients group. According to the sequencing results, L. reuteri, which was one of the dominant Lactobacillus species in the patient group, could not be detected in healthy controls. Bifidobacterium infantis was found in the patients' feces but not in the controls. We demonstrated a BMI and age-independent association between the presence of NASH and levels of A. muciniphila and Enterobacteriaceae as well as increased endotoxin levels. L. reuteri was abundant in the patient group, suggesting that dominant Lactobacillus species should be considered before probiotic treatments.

Gastrointestinal endotoxin and metabolic responses in cows fed and recovered from two different grain-rich challenges

Effects of two grain-rich feeding challenges and their subsequent recovery on gastrointestinal endotoxin concentrations, acute phase response, and blood metabolites were determined in eight rumen-cannulated, non-lactating Holstein cows. A 2 × 2 cross-over design was used. At the start of the experiment, cows were fed forage-only diet (baseline, d 0) and after a 6-d gradual adaptation, challenged with a 60% grain diet for 4 wk (d 7 – 35), either continuously (CONT) or interruptedly with a 1-wk break in the second wk (INT). Subsequently, cows were fed the forage-only diet for 9 wk to evaluate the recovery of the grain challenges. Feeding challenges markedly increased ruminal and fecal endotoxin concentrations, which returned to the baseline levels during the recovery phase. Ruminal endotoxin concentration tended to be higher in CONT than in INT cows on d 14 and 25. The concentration of acute phase proteins serum amyloid A and haptoglobin were not affected by the feeding challenges. The level of the liver enzyme aspartate aminotransferase was transiently increased on d 14 and 25 only in the CONT cows. The concentration of glutamate dehydrogenase peaked on d 14 of both challenge models and lowered thereafter. Blood glucose and urea concentrations rose due to the challenges with glucose tending to be higher in INT than in CONT cows. Both feeding challenges lowered blood cholesterol, non-esterified fatty acids, and creatinine concentrations. In conclusion, the feeding challenges promoted endotoxin release in the rumen and hindgut but did not trigger an acute phase response. All altered variables returned to baseline values within 2 wk after the both interruptedly and continuously high-grain feeding.

Intestinal dysbiosis contributes to the delayed gastrointestinal transit in high-fat diet fed mice.

Background & AimsHigh-fat diet (HFD) feeding is associated with gastrointestinal motility disorders. We recently reported delayed colonic motility in mice fed a HFD for 11 weeks. In this study, we investigated the contributing role of gut microbiota in HFD-induced gut dysmotility.MethodsMale C57BL/6 mice were fed a HFD (60% kcal fat) or a regular/control diet (RD) (18% kcal fat) for 13 weeks. Serum and fecal endotoxin levels were measured, and relative amounts of specific gut bacteria in the feces were assessed by real-time polymerase chain reaction. Intestinal transit was measured by fluorescent-labeled marker and a bead expulsion test. Enteric neurons were assessed by immunostaining. Oligofructose (OFS) supplementation with RD or HFD for 5 weeks also was studied. In vitro studies were performed using primary enteric neurons and an enteric neuronal cell line.ResultsHFD-fed mice had reduced numbers of enteric nitrergic neurons and showed delayed gastrointestinal transit compared with RD-fed mice. HFD-fed mice had higher fecal Firmicutes and Escherichia coli and lower Bacteroidetes compared with RD-fed mice. OFS supplementation protected against enteric nitrergic neuron loss in HFD-fed mice, and improved intestinal transit time. OFS supplementation resulted in a reduction in fecal Firmicutes and Escherichia coli and serum endotoxin levels. In vitro, palmitate activation of TLR4 induced enteric neuronal apoptosis in a Phospho–c-Jun N-terminal kinase–dependent pathway. This apoptosis was prevented by a c-Jun N-terminal kinase inhibitor and in neurons from TLR4-/- mice.ConclusionsTogether our data suggest that intestinal dysbiosis in HFD-fed mice contribute to the delayed intestinal motility by inducing a TLR4-dependent neuronal loss. Manipulation of gut microbiota with OFS improved intestinal motility in HFD mice.

High Fat Diet-Induced Gut Microbiota Exacerbates Inflammation and Obesity in Mice via the TLR4 Signaling Pathway

Background & AimsWhile it is widely accepted that obesity is associated with low-grade systemic inflammation, the molecular origin of the inflammation remains unknown. Here, we investigated the effect of endotoxin-induced inflammation via TLR4 signaling pathway at both systemic and intestinal levels in response to a high-fat diet.MethodsC57BL/6J and TLR4-deficient C57BL/10ScNJ mice were maintained on a low-fat (10 kcal % fat) diet (LFD) or a high–fat (60 kcal % fat) diet (HFD) for 8 weeks.ResultsHFD induced macrophage infiltration and inflammation in the adipose tissue, as well as an increase in the circulating proinflammatory cytokines. HFD increased both plasma and fecal endotoxin levels and resulted in dysregulation of the gut microbiota by increasing the Firmicutes to Bacteriodetes ratio. HFD induced the growth of Enterobecteriaceae and the production of endotoxin in vitro. Furthermore, HFD induced colonic inflammation, including the increased expression of proinflammatory cytokines, the induction of Toll-like receptor 4 (TLR4), iNOS, COX-2, and the activation of NF-κB in the colon. HFD reduced the expression of tight junction-associated proteins claudin-1 and occludin in the colon. HFD mice demonstrated higher levels of Akt and FOXO3 phosphorylation in the colon compared to the LFD mice. While the body weight of HFD-fed mice was significantly increased in both TLR4-deficient and wild type mice, the epididymal fat weight and plasma endotoxin level of HFD-fed TLR4-deficient mice were 69% and 18% of HFD-fed wild type mice, respectively. Furthermore, HFD did not increase the proinflammatory cytokine levels in TLR4-deficient mice.ConclusionsHFD induces inflammation by increasing endotoxin levels in the intestinal lumen as well as in the plasma by altering the gut microbiota composition and increasing its intestinal permeability through the induction of TLR4, thereby accelerating obesity.

Chronic administration of dietary grape seed extract increases colonic expression of gut tight junction protein occludin and reduces fecal calprotectin: a secondary analysis of healthy Wistar Furth rats

Animal studies have demonstrated the potential of grape seed extract (GSE) to prevent metabolic syndrome, obesity, and type 2 diabetes. Recently, metabolic endotoxemia induced by bacterial endotoxins produced in the colon has emerged as a possible factor in the etiology of metabolic syndrome. Improving colonic barrier function may control endotoxemia by reducing endotoxin uptake. However, the impact of GSE on colonic barrier integrity and endotoxin uptake has not been evaluated. We performed a secondary analysis of samples collected from a chronic GSE feeding study with pharmacokinetic end points to examine potential modulation of biomarkers of colonic integrity and endotoxin uptake. We hypothesized that a secondary analysis would indicate that chronic GSE administration increases colonic expression of intestinal tight junction proteins and reduces circulating endotoxin levels, even in the absence of an obesity-promoting stimulus. Wistar Furth rats were administered drinking water containing 0.1% GSE for 21 days. Grape seed extract significantly increased the expression of gut junction protein occludin in the proximal colon and reduced fecal levels of the neutrophil protein calprotectin, compared with control. Grape seed extract did not significantly reduce serum or fecal endotoxin levels compared with control, although the variability in serum levels was widely increased by GSE. These data suggest that the improvement of gut barrier integrity and potential modulation of endotoxemia warrant investigation as a possible mechanism by which GSE prevents metabolic syndrome and associated diseases. Further investigation of this mechanism in high-fat feeding metabolic syndrome and obesity models is therefore justified.

Free endotoxins in the feces of lactating dairy cows

A survey was conducted on 300 lactating dairy cows on 10 dairy farms to determine how risk factors for and symptoms of excessive grain feeding and subacute ruminal acidosis are associated with the concentrations of endotoxins in feces measured with the Limulus amoebocyte lysate test. Increases in days in milk and haptoglobin in blood plasma were associated with lower (P = 0.02) and higher (P = 0.02) fecal endotoxin, respectively. The five farms with a dietary neutral detergent fibre (NDF) content higher than 33.8% of DM had lower (P &lt; 0.01) fecal endotoxin than those with a dietary NDF content lower than 33.8% of DM (31 790 vs. 69 276 endotoxin units (EU) g-1 of wet feces, P &lt; 0.01). Parity, milk yield, milk fat percentage, milk protein percentage, the blood plasma concentration of serum amyloid A, and the dietary content of physically effective fibre were not associated with the fecal endotoxin concentration.

IgA against gut-derived endotoxins: does it contribute to suppression of hepatic inflammation in alcohol-induced liver disease?

Endotoxins of intestinal origin are supposed to play an important role in the development of alcoholic hepatitis in man. To estimate the role of immunoglobulin response to gut-derived endotoxin in the development of alcohol-induced liver disease, serum levels of IgA and IgG against fecal endotoxin, endotoxin, and acute-phase proteins were measured in patients with different stages of alcoholic liver disease and in healthy controls. Antibodies of type IgA, but not IgG, against fecal endotoxins were significantly increased in patients with alcohol-induced liver disease. IgA antibodies against fecal endotoxin were found to be closely correlated with the plasma concentrations of alanine aminotransferase, gamma-glutamyl transferase, and C-reactive protein in patients with alcoholic liver disease. In conclusion, as IgA located in body tissue was shown to suppress the inflammatory process, enhanced production of IgA against endotoxin of intestinal origin may contribute to inactivation of this compound, thereby reducing its damaging effect on the liver.

Plasma antibodies against fecal endotoxin of type IgA, but not IgG are elevated in patients with alcohol-induced liver disease

Plasma antibodies against fecal endotoxin of type IgA, but not IgG are elevated in patients with alcohol-induced liver disease

Plasma antibodies against fecal endotoxin of type IGA, but not IGG are elevated in patients with alcohol-induced liver disease

Plasma antibodies against fecal endotoxin of type IGA, but not IGG are elevated in patients with alcohol-induced liver disease

Role of gut-derived endotoxaemia and bacterial translocation in rats after thermal injury: effects of selective decontamination of the digestive tract

This study was performed to investigate: (1) the role of gut-derived endotoxin/bacterial translocation in the pathogenesis of sepsis, and (2) the possible effects of selective decontamination of the digestive tract (SDD) on mortality in rats following 40 per cent full-thickness scald injury. In the SDD-treated group, Enterobacteriaceae and yeasts were eradicated from the caecal mucosa, while the mucosal flora consisting of mainly anaerobes was well preserved, within 3 days. The incidence of bacterial translocation to the mesenteric lymph nodes (MLN) and viscerae was significantly lowered on postburn days 1, 3 and 5 ( P < 0.05−0.01). Meanwhile, pretreatment with SDD resulted in reductions of the faecal endotoxin levels in different segments of intestinal tract to less than 0.5 per cent (0.04 – 0.45 per cent) of the untreated control; there was also a significant attenuation of the elevation of endotoxin concentrations in both portal and systemic blood. Intestinal diamine oxidase (DAO) activity returned to baseline on day 5 in rats receiving SDD but not in controls. The 5-day survival rate in the SDD-treated group was elevated by 26.7 per cent as compared with controls ( P < 0.05). These data suggested that endotoxin/bacterial translocation took place early and commonly, which in turn contributed to postburn sepsis and mortality. SDD was effective in preventing gut origin endotoxaemia and bacterial translocation, and improving the survival rate in rats following severe thermal injuries.

Gut-derived endotoxemia and multiple system organ failure following gunshot wounds combined with hemorrhagic shock: an experimental study in the dog.

The purpose of this study was to explore the causative effects of high-velocity bullet injury (5.56 mm, 930 m/sec) combined with hemorrhagic shock on gut-derived endotoxemia and multiple system organ dysfunction or failure. The concentration of endotoxin in both portal and systemic blood was markedly increased after gunshot wounds together with hemorrhagic shock (p < 0.05-0.01). The portal/systemic lipopolysaccharide ratio persistently decreased in the combined wound (CW) group at 24 to 72 hours after injury, and it was much lower in the CW group than that in the single gunshot wound (SW) group. Also, a significant increase of fecal endotoxin content was found in the CW group as compared to the SW group (118.30 +/- 75.36 vs. 8.89 +/- 3.32 micrograms/g, p < 0.01), which was paralleled with the population of gram-negative bacilli in the intestinal tract. The incidence of multiple system organ failure, multiorgan dysfunction (including single organ failure) in the CW group were 30.8% (4 of 13) and 38.5% (5 of 13), respectively. These results suggested that severe trauma could lead to gut origin endotoxemia and bacterial translocation, which might play an important role in the pathogenesis of sepsis and multiple system organ failure following gunshot wounds.

Faecal Endotoxin in Human Volunteers: Normal Values

This paper presents a study measuring endotoxin levels in faeces of healthy adults using the Limulus amoebocyte lysate (LAL) microassay. Data showed mean faecal endotoxin levels of 1 mg (range 0.01-100 mg) per gram of faeces. No correlation was found with the concentration of Enterobacteriaceae in faeces and free Faecal endotoxin levels. Keywords: Endotoxin; LAL micro-assay; LPS; Faeccs; Human volunteers: Enterobacteriaceae.