PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “LIPOPOLYSACCHARIDES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,063 records · Page 59Linked to original sources

Responses of serum lipids and adipose tissue lipases to lipopolysaccharide administration in normal and hepatoma-bearing rats.

The effects of in vivo lipopolysaccharide administration on serum lipid metabolism were studied in normal and hepatoma-bearing rats. Changes in serum lipid levels and adipose tissue lipase (lipoprotein lipase and hormone-sensitive lipase) activities following injection of lipopolysaccharide into normal rats resembled those in hepatoma-bearing rats. These results suggest the presence of some common factor(s) involved in the incidence of abnormal lipid metabolism upon lipopolysaccharide injection and hepatoma transplantation.

Adipose Tissue↗

Structural studies on the core oligosaccharide of Phenylobacterium immobile strain K2 lipopolysaccharide. Chemical synthesis of 3-hydroxy-5c-dodecenoic acid.

The fatty acid composition of the bound lipids of 17 strains from Phenylobacterium immobile was investigated. Ester-linked 3-hydroxy-5c-dodecenoic acid was found to be the major substituent in the lipopolysaccharide. Therefore the occurrence of this unusual acid can be taken as a useful marker for the determination of P. immobile by simple fatty acid analysis. Lipid A backbone was found to consist of 2,3-diamino-2,3-dideoxy-D-glucose, which up to this time has only been detected in group I of purple nonsulfur bacteria and their non-phototrophic relatives. A convenient chemical synthesis for 3-hydroxy-5c-dodecenoic acid is described. The polysaccharide region of P. immobile strain K2 lipopolysaccharide was investigated. The methods used included gel filtration procedures, methylation analysis, periodate oxidation, Smith degradation, oxidation with chromium trioxide and enzymic degradations of the isolated oligosaccharide. We found that strain K2 has a rough-type lipopolysaccharide, devoid of an O-specific side chain. For the core oligosaccharide the following structure is proposed: (Formula: see text) beta-D-Glcp(1-3)-L-alpha-D-Hep rho(1-3)-L-alpha-D-Hep rho(1-3-L-alpha-D-Hep rho(1-4/5)dOclA.

Carbohydrate Conformation↗

Tumour necrosis factor-alpha and lipopolysaccharide enhance interferon-induced tryptophan degradation and pteridine synthesis in human cells.

The capacity of recombinant interferon-alpha, -beta and -gamma, of bacterial lipopolysaccharide and of recombinant tumour necrosis factor-alpha to induce indoleamine 2,3-dioxygenase and synthesis of pteridines was studied in human peripheral blood mononuclear cells, human macrophages and normal dermal fibroblasts. The action of interferon-alpha and -beta on macrophages was supported by lymphocyte factors as indicated by the effect of these mediators in the absence or presence of lymphocytes. Tumour necrosis factor-alpha alone was ineffective in peripheral blood mononuclear cells and macrophages, but it significantly increased the action of all three interferon species on macrophages and fibroblasts. Lipopolysaccharide directly affected macrophages or dermal fibroblasts and enhanced the effect of interferon-gamma. However, in the presence of lymphocytes, the action of lipopolysaccharide was mediated via interferon-gamma.

Biopterins↗

Effects of fish oil supplementation on the performance and the immunological, adrenal, and somatotropic responses of weaned pigs after an Escherichia coli lipopolysaccharide challenge.

Seventy-two crossbred pigs (7.58 +/- 0.30 kg BW) weaned at 28 +/- 3 d of age were used to investigate the effects of fish oil supplementation on pig performance and on immunological, adrenal, and somatotropic responses following an Escherichia coli lipopolysaccharide (LPS) challenge in a 2 x 2 factorial design. The main factors consisted of diet (7% corn oil [CO] or 7% fish oil [FO]) and immunological challenge (LPS or saline). On d 14 and 21, pigs were injected intraperitoneally with either 200 microg/kg BW of LPS or an equivalent amount of sterile saline. Blood samples were collected 3 h after injection for analysis of interleukin-1beta (IL-1beta), prostaglandin E2 (PGE2), cortisol, growth hormone (GH), and insulin-like growth factor (IGF)-I. On d 2 after LPS challenge, peripheral blood lymphocyte proliferation (PBLP) was determined. Lipopolysaccharide challenge decreased ADG (487 vs. 586 g; P < 0.05) and ADFI (as-fed, 776 vs. 920 g; P < 0.05) from d 14 to 21 and ADG (587 vs. 652 g; P < 0.10) from d 21 to 28. Fish oil improved ADG (554 vs. 520 g; P < 0.10) and ADFI (891 vs. 805 g; P < 0.10) from d 14 to 21. On d 14, LPS challenge x diet interactions were observed for IL-1beta (P < 0.10), PGE2 (P < 0.001), and cortisol (P < 0.05) such that these measurements responded to the LPS challenge to a lesser extent (IL-1beta: 93 vs. 114 pg/mL, P < 0.05; PGE2: 536 vs. 1,285 pg/mL, P < 0.001; cortisol: 143 vs. 206 ng/mL, P < 0.05) in pigs receiving the FO diet than in pigs fed the CO diet. In contrast, among LPS-treated pigs, pigs fed the FO diet had higher IGF-I (155 vs. 101 ng/mL; P < 0.10) than those fed the CO diet. On d 21 among LPS-treated pigs, pigs fed FO had lower IL-1beta (70 vs. 84 pg/mL; P < 0.10) and cortisol (153 vs. 205 ng/mL; P < 0.05) than those fed CO. Pigs fed FO had lower PGE2 (331 vs. 444 pg/mL; P < 0.05) and higher IGF-I (202 vs. 171 ng/mL; P < 0.10) compared with those fed CO. Lipopolysaccharide challenge decreased GH (0.27 vs. 0.33 ng/mL; P < 0.05) on d 14, whereas it had no effect on GH on d 21. During both LPS challenge periods, the challenge increased PBLP when these cells were incubated with 8 (1.46 vs. 1.32; P < 0.10) or 16 microg/mL (1.46 vs. 1.30; P < 0.05) of concanavalin A. Fish oil had no effect on PBLP. These results suggest that FO alters the release of proinflammatory cytokines, which might lead to improved pig performance during an immunological challenge.

Animals↗

Effects of lipopolysaccharide and phenylbutazone on gastric contents in the horse.

REASONS FOR PERFORMING STUDY: Endotoxaemia causes a disruption of gastrointestinal motility in the horse but there is no information on its effects on gastric secretion. Lipopolysaccharide (LPS) administration is known to affect gastric secretion in other species. HYPOTHESIS: That LPS, a toxic component of Gram-negative bacteria, would reduce gastric acid secretion and that pretreatment with phenylbutazone (PBZ) would block the effects of LPS. METHODS: The effects of LPS and PBZ on gastric contents were investigated in fasted, mature horses, with permanent gastric cannulae. Horses were pretreated with either saline or PBZ 15 mins before a 60 min infusion of either LPS or saline. Gastric contents were collected at 15 min intervals for 3 h, beginning 15 mins after the start of the LPS or saline infusion. RESULTS: Lipopolysaccharide significantly decreased gastric acid output, [K+] and potassium output and increased [Na+] and sodium output. Phenylbutazone did not affect basal gastric acid secretion but decreased LPS-induced changes in the secreted volume, [Na+] and sodium output. CONCLUSIONS: This study provides evidence that LPS affects gastric acid secretion in the horse and that these LPS-induced changes are mediated, in part, by prostaglandins. POTENTIAL RELEVANCE: Lipopolysaccharide administration can induce changes in the composition of gastric contents in the horse but further work is needed to determine the source of these changes.

Animals↗

Quality assessment of pasteurized fluid milk as related to lipopolysaccharide content.

A study was conducted to investigate any relationship between lipopolysaccharide (endotoxin) concentration in milk and parameters associated with the keeping quality of milk. Parameters investigated were flavor intensity, standard plate count, coliform count, psychrotrophic count, and gram-negative count. Lipopolysaccharide content was determined using the Limulus Amoebocyte Lysate assay. Pasteurized whole milk samples were obtained the day of processing in .94-L containers with samples analyzed on d 0 through 21. Significant linear relationships were detected between lipopolysaccharide concentration and days storage at 7 degrees C, flavor intensity, and psychrotrophic count.

Animals↗

Concentrations of alpha-Tocopherol after intramammary infusion of Escherichia coli or lipopolysaccharide.

Fifteen Holstein cows were used in a trial involving intramammary challenge to determine the effects of acute clinical mastitis on the concentrations of alpha-tocopherol in milk and plasma and the concentrations of neutrophils in milk and blood. Cows were assigned to one of three experimental groups challenged by intramammary infusion of lipopolysaccharide, Escherichia coli, or sterile phosphate-buffered saline. All quarters infused with lipopolysaccharide or E. coli were diagnosed with clinical mastitis on d 1 and 2 after challenge. Acute inflammation caused by intramammary infusion of lipopolysaccharide or E. coli resulted in increased concentrations of alpha-tocopherol in milk in challenged quarters but had no effect on concentrations of alpha-tocopherol in plasma. Concentrations of alpha-tocopherol in milk and blood neutrophils did not differ among treatment groups. Concentrations of alpha-tocopherol did not differ between milk and blood neutrophils. Approximately 25% of the alpha-tocopherol in milk from glands with clinical mastitis was associated with neutrophils, and < 10% of the alpha-tocopherol in milk from nonmastitic glands was associated with neutrophils. A shift toward sources of alpha-tocopherol other than synthesized milk fat occurred during acute inflammation in the mammary gland.

Animals↗

Local immune response in experimental pyelonephritis in the rabbit. II. Lymphocyte stimulation by lipopolysaccharide of infecting organism.

The response of circulating and kidney lymphocytes from rabbits with experimental haematogenous pyelonephritis to somatic (O) antigen (lipopolysaccharide) from the infecting organism was evaluated. Lymphocytes were cultured for 3 days in the presence and absence of lipopolysaccharide from the infecting organism, Escherichia coli O75 and a heterologous organism. Circulating lymphocytes showed a significant response to the homologous lipopolysaccharide by day 5 of infection, and kidney lymphocytes responded by day 19 of infection but failed to respond after day 33. The lipid moiety of somatic antigen was required for the stimulation of lymphocytes since antigen preparations in which lipid was low or absent did not activate lymphocytes. B lymphocytes from kidney were stimulated by this antigen whereas both T and B circulating lymphocytes responded. Thus, pyelonephritis in rabbits is associated with the activation of a subpopulation of circulating cells which have specific receptors for the homologous antigen. B lymphocytes that are specifically activated by the homologous or O antigen then localize to the infected site.

Animals↗

Structural requirements for intracellular processing and sorting of bactericidal/permeability-increasing protein (BPI): comparison with lipopolysaccharide-binding protein.

The bactericidal/permeability-increasing protein (BPI), which is stored in the azurophil granules of neutrophils, and the circulating lipopolysaccharide-binding protein (LBP) share the same structure. Both bind lipopolysaccharide of gram-negative bacteria through their amino-terminal domains. The carboxy-terminal domain of BPI promotes bacterial attachment to phagocytes, whereas the corresponding domain of LBP delivers lipopolysaccharide to monocytes/macrophages. Our aim was to investigate the role of the amino-and carboxy-terminal domains of BPI and LBP for sorting and storage in myeloid cells after transfection of cDNA to two rodent hematopoietic cell lines. Full-length BPI and LBP were both targeted for storage in these cells. Deletion of the carboxy-terminal half of BPI resulted in storage followed by degradation while the reciprocal deletion of the amino-terminal half led to retention in the endoplasmic reticulum for proteasomal degradation. Chimeras between halves of BPI and LBP were also targeted for storage, but those containing carboxy-terminal BPI had the highest stability, again indicating a role for the carboxy-terminal domain of BPI in protection against degradation. Therefore, we propose a critical stability function for the hydrophobic carboxy-terminal domain of BPI during intracellular sorting for storage while the amino-terminal domain may confer targeting for storage.

Acute-Phase Proteins↗

Production of interleukin-1 receptor antagonist isoforms by microglia in mixed rat glial cells stimulated by lipopolysaccharide.

Although the natural interleukin-1 receptor antagonist (IL-1Ra) has been shown to be produced by microglial cells in response to immune stimuli, nothing was known about the ability of these cells in primary culture to produce the different isoforms of IL-1Ra. Using RT-PCR, we first confirmed that mixed glial cell cultures from newborn rats respond to the cytokine inducer, lipopolysaccharide, by synthesizing IL-1Ra mRNA. Using double immunostaining, we showed that IL-1Ra was detected in microglia but not in astrocytes. Using Western blotting, we finally demonstrated that the IL-1Ra1 isoform was secreted in the supernatant of mixed glial cell cultures, and its production increased in response to lipopolysaccharide. The three different IL-1Ra isoforms were constitutively expressed in cell lysates and their levels increased after lipopolysaccharide treatment, except for IL-1Ra3. These results point to the ability of microglial cells in primary culture to produce the different isoforms of IL-1Ra.

Animals↗

Up-regulation of gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide by aspirin but not indomethacin.

Infection with Helicobacter pylori and the use of non-steroidal anti-inflammatory drugs (NSAIDs) are recognized as the two primary factors in the etiology of gastric disease. In this study, we applied the animal model of H. pylori-induced gastritis to assess the influence of NSAIDs on the course of mucosal inflammatory responses to H. pylori. Two days following intragastric application of H. pylori lipopolysaccharide, rats were divided into groups and administered daily for up to 8 days either indomethacin, aspirin or the vehicle, and their gastric mucosal tissue subjected to histological and biochemical assessment. H. pylori lipopolysaccharide elicited within 2 days a pattern of acute mucosal inflammatory responses accompanied by a massive epithelial cell apoptosis, and a marked increase in the expression of membrane-bound and soluble forms of TNF-alpha. The extent of mucosal inflammatory involvement reached a maximum by the 4th day and showed a decline by the 10th day; this was reflected in a 38.1% reduction in apoptosis, a 53.2% decline in membrane-bound TNF-alpha and a 63.8% decrease in soluble TNF-alpha. Compared to the vehicle controls, aspirin caused a 36.2% increase in the severity of the mucosal inflammatory involvement by the second day of administration and a 25.9% increase in the inflammatory involvement occurred by the 8th day; this effect of aspirin was accompanied by a significant (54.5%) induction in apoptosis, a 58.2% decline in membrane-bound TNF-alpha and a 61% increase in soluble TNF-alpha. In contrast, administration of indomethacin evoked only a marginal increase (5-7%) in apoptosis, and caused no discernible changes in the severity of gastric mucosal involvement and the expression of TNF-alpha forms elicited by H. pylori lipopolysaccharide. The findings indicate that aspirin, but not indomethacin, increases the severity of gastric mucosal inflammatory responses to H. pylori. This detrimental influence of aspirin appears to result from up-regulation in the mucosal expression of soluble form of TNF-alpha, which leads to the amplification of apoptotic events that potentiate gastric mucosal inflammatory reaction to H. pylori.

Animals↗

Changes in some factors of the innate immunity and serum zinc and iron concentrations in pigs following intravenous administration of Escherichia coli lipopolysaccharide.

The changes in some factors of the innate immunity (phagocytosis, complement, lysozyme); haematological parameters-leukocytes, erythrocytes, differential white blood cell counts, haemoglobin, haematocrit and the serum concentrations of the microelements zinc and iron in six 2- to 3-months-old female piglets after the intravenous administration of lipopolysaccharide from Escherichia coli 0111:B4 were determined. It was found out that 1 h after the administration of lipopolysaccharide at the dosage rate of 10 microg/kg body weight resulted in a decrease in the phagocytic parameters, i.e. the phagocytic number and the index of phagocytic activity, which was followed by an increase in their values between post treatment hours 2 and 4. The leukocyte counts had decreased by hour 2 after the injection, but thereafter increased, and at post treatment hour 72, a leukocytosis was observed. The differential white blood cell counts were characterized by a shift to the left between hours 2 and 4 and a statistically significant increase in lymphocyte counts at hour 48 of the experiment. The serum zinc concentrations were increased an hour after the lipopolysaccharide application; after which their average values were lower. The haemolytic activities (CH50) of the classical and the alternative pathways of complement activation decreased. The haemolytic activity (CH50) for the classical pathway began to increase at hour 48 following the treatment. Significant changes were not observed in lysozyme activity, serum iron concentrations or the related haematological parameters (erythrocytes and haemoglobin).

Animals↗

The biological activity of a liposomal complete core lipopolysaccharide vaccine.

A vaccine that induces humoral immunity to lipopolysaccharide (LPS), while remaining non-pyrogenic should be beneficial, as high levels of antibodies against LPS are associated with a reduced risk of adverse outcome. However, pure LPS or bacteria expressing LPS are generally considered too toxic to be used as vaccines. Recently, a novel, immunogenic complete core lipopolysaccharide vaccine has been described, which has been designed to prevent endotoxin-related inflammatory reactions in surgical and high-risk hospitalized patients. In vivo studies have shown that while administration of the vaccine to rabbits results in no toxicity over 7 days, it does induce significantly enhanced antibody responses towards a broad range of clinically relevant Gram-negative LPSs. Here we show that encapsulation of the four complete core LPS types Escherichia coli K12, Escherichia coli R1, Bacteroides fragilis and Pseudomonas aeruginosa into liposomes greatly reduces the ability of a given amount of LPS to induce TNF-alpha production in vitro from human monocytes. In contrast to previous studies of liposomal LPS, we demonstrate a reduction in activity of approximately 100,000-fold; a reduction approximately 100-1,000-fold more than that previously described. The signalling by the liposomal LPS appears to be entirely dependent on serum factors, though this can be partially restored by soluble CD14 or, to a lesser extent, by lipopolysaccharide binding protein. Time-course experiments reveal that liposomal LPS signalling shows similar kinetics to pure LPS signalling. Therefore, as well as inducing specific antibody responses, liposomal LPS demonstrates characteristics suitable for use as a vaccine to be used in human beings.

Animals↗

Lipopolysaccharides from Mesorhizobium huakuii and Mesorhizobium ciceri: chemical and immunological comparative data.

Lipopolysaccharides of two Mesorhizobium species of different host specificity were compared: M. huakuii and M. ciceri. M. huakuii sp. was represented by five strains with special consideration of M. huakuii IFO 15243(T). SDS/PAGE profiles revealed that all M. huakuii LPS preparations contained low molecular mass fractions (LPS-II) of the same molecular size. All of lipopolysaccharides contained high molecular mass fractions (LPS-I). However, the high molecular mass fraction from each strain possessed an individual molecular size distribution pattern. The crossreactivity of blotted lipopolysaccharides with rabbit polyclonal antibodies against Mesorhizobium huakuii IFO 15243(T) whole bacteria indicated the presence of common epitope(s) within the investigated Mesorhizobium huakuii strains. Moreover, LPS from M. huakuii S52 also reacted with anti M. ciceri HAMBI 1750 serum showing that there are epitopes common for different mesorhizobial species. LPS isolated from Mesorhizobium huakuii strain IFO 15243(T) contained neutral sugars: L-6-deoxytalose, L-rhamnose, D-galactose and D-glucose, aminosugars:D-quinovosamine, D-glucosamine, D-2,3-diamino-2,3-dideoxyglucose and D-galacturonic and D-glucuronic acids. In the LPS preparation, fatty acids typical for Mesorhizobium strains were detected. 3-Hydroxydodecanoic, 3-hydroxy-iso-tridecanoic, 3-hydroxyeicosanoic, 3-hydroxyheneicosanoic and 3-hydroxydocosenoic acids were the major amide linked fatty acids, while iso -heptadecanoic, eicosanoic, docosenoic, as well as 27-hydroxyoctacosanoic and 27-oxooctacosanoic acids were the dominant ester linked fatty residues.

Alphaproteobacteria↗

The effect of systemic administration of lipopolysaccharide on cerebral haemodynamics and oxygenation in the 0.65 gestation ovine fetus in utero.

OBJECTIVE: To investigate the effect of intravenous lipopolysaccharide on systemic and cerebral haemodynamics and oxygenation in the preterm ovine fetus. DESIGN: Prospective observational study. SETTING: Research centre for perinatal brain injury. SAMPLE: Nine fetal sheep at circa 93 days of gestation (0.65). METHODS: Fetal sheep were chronically instrumented with arterial and venous catheters and a flow probe in the carotid artery. Near-infrared spectroscopy was used to measure changes in cerebral oxygenation and total haemoglobin concentration. Three days after surgery, each fetus was given 100 ng/kg Escherichia coli lipopolysaccharide. Observations were continued for 48 hours post-injection and compared with baseline control values. MAIN OUTCOME MEASURES: Fetal heart rate, mean arterial pressure, carotid blood flow. RESULTS: Three fetuses died after administration of the lipopolysaccharide. In the survivors fetal heart rate rose from 193 (SEM 7) to a mean maximal level of 226 (SEM 31 bpm) (P = 0.01) after 6.5 (SEM 1.0) hours. The mean arterial pressure decreased from 40.5 (SEM 4.2) to 29.4 (SEM 1.6) mmHg (P < 0.05) after 7.0 (SEM 2.0) hours, and carotid blood flow increased from 29.6 (SEM 1.6) to 45.8 (SEM 5.7) mL/min (P = 0.0002) at 12 (SEM 3) hours. All values returned to control levels by 48 hours. Histological assessment showed evidence of periventricular leucomalacia in three out of six brains studied. CONCLUSION: These data do not suggest that cerebral ischaemia is the main aetiological factor in endotoxin-related fetal brain injury. Fetal tachycardia and cerebral vasodilation may indicate endotoxaemia in fetuses exposed to prenatal infection.

Animals↗

[Effect of the lipopolysaccharide-protein complex of Pseudomonas syringae PV. atrofaciens on the process of tumor formation caused by Agrobacterium tumefaciens].

It has been found that the agent of bacterial spotting of rye P. syringae pv. atrofaciens 8281 has no antagonistic action on the strains 9052 and 9054 of Agrobacterium tumefaciens--the agent of crown gall tumor. Lipopolysaccharide-protein complex of P. syringae pv. atrofaciens 8281 when added to the culture medium does not affect the growth and development of A. tumefaciens bacteria. It has been experimentally established that the lipopolysaccharide-protein complex of P. syringae pv. atrofaciens 8281, when used to treat the potato explants before inoculation of A. tumefaciens, decreases induction and development of tumours on the explants. Tumour formation inhibition depends on concentration of lipopolysaccharide-protein complex solution.

Agrobacterium tumefaciens↗

[Ivermectin inhibits activation of Kupffer cells induced by lipopolysaccharide toxin].

Lipopolysaccharide-stimulated liver macrophages (Kupffer cells) secrete many physiologically active substances responsible for inflammatory reaction of the organism. The mechanism by which ivermectin, a macrocyclic lactone possessing a broad antiparasitic activity, modulates basic effects elicited by lipopolysaccharide in the primary culture of rat Kupffer cells was studied. It was found that ivermectin in the absence of endotoxin did not affect a functional state of the Kupffer cells. Preincubation of Kupffer cells with ivermectin (1 mM), however, significantly blocked response to the subsequent administration of lipopolysaccharide (1 mg/ml). In particular, secretion of tumor necrosis factor TNF alpha, nitric oxide NO and prostaglandin E2 was suppressed. Also, an LPS-triggered rise in the intracellular concentration of calcium ions was less pronounced. Removal of chloride anions from the extracellular medium completely abolished inhibitory effects of ivermectin. It is suggested that invermectin exerts its action via binding to the glycine-gated chloride receptors/channels of the Kupffer cells, which may reduce toxic reactions manifestations observed under infections caused by Gram-negative bacteria.

Animals↗

[Biological activity of lipopolysaccharides from clinical Bacteroides fragilis strains isolated in Poland determined in reaction with limulus amoebocyte lysate].

The aim of this study was to determine a biological activity of lipopolysaccharides (LPS) from clinical Bacterioides fragilis strains isolated in Poland by means of quantitative, photometric BET (LAL) method with Limulus polyphemus amoebocyte lysate and chromogenic substrate S-2423. Lipopolysaccharides were extracted from nine clinical B. fragilis strains by the procedure of Westphal and Jann (1965). Crude LPS preparations were purified with ultracentrifugation. Biological activities of bacterial endotoxins were determined by quantitative BET method with chromogenic substrate S-2423 (ENDOCHROME kit). Tests were performed according to the recommendations of the producer (Charles River Endosafe Ltd., USA). E. coli O55:B5 LPS and LPS preparations from reference B. fragilis strains were applied to compare the results of examinations. Activities of endotoxins from clinical B. fragilis strains isolated in Poland determined in reaction with Limulus amoebocyte lysate were differentiated. Among endotoxins of clinical B. fragilis strains the most active was the preparation from strain cultured in the case of pancreatic ulcer (B. fragilis 80/81 LPS). Lipopolysaccharides of examined B. fragilis strains were less active in BET test than E. coli O55:B5 LPS.

Bacteroides fragilis↗