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PubMed1994

Immunoenzymometric analysis for expression and shedding of intercellular adhesion molecule-1 on human endothelial cells stimulated with cytokines or lipopolysaccharide.

Unstimulated endothelial cell (EC) cultures express low levels of intercellular adhesion molecule-1 (ICAM-1) and their expression can be enhanced by inflammatory cytokines such as tumor necrosis factor alpha (TNF). Three monoclonal antibodies (MoAbs) highly reactive with TNF-stimulated human ECs were established and defined to recognize a 95 kDa cell surface protein specifically expressed on cytokine-activated ECs, which was immunochemically identified as ICAM-1. The quantitative immunoassay of soluble and insoluble ICAM-1 could be performed with two different MoAbs. Secretion of fibronectin or the von Willebrand factor, was not significantly enhanced with TNF stimulation. Cellular expression of ICAM-1 was drastically induced by TNF or interleukin-1 stimulation, and the moderate expression with delayed-action was observed only by lipopolysaccharide stimulation. A maximal amount of soluble ICAM-1 was released from ECs stimulated only by TNF, apparently in a dose dependent manner, but no significant release of ICAM-1 was induced by thrombin interleukin-2, or lipopolysaccharides. Released levels of soluble ICAM-1 from interleukin-1-stimulated ECs were apparently diminished as compared with those from TNF-stimulated cells. These results suggest that release of soluble ICAM-1 from EC surfaces can be most significantly enhanced by TNF-specific signaling, and prospectively, should be a sensitive indicator of intravascular inflammation in acute endothelium injury.

Antibodies, Monoclonal↗

PubMed1981

Studies on isolated gut mucosal lymphocytes in inflammatory bowel disease. Detection of activated T cells and enhanced proliferation to Staphylococcus aureus and lipopolysaccharides.

To determine whether a defective proliferation of gut mucosal lymphocytes is a contributory factor to the pathogenesis of inflammatory bowel disease, we assessed their reactivity toward mitogens and bacterial antigens. Spontaneous replication of intestinal lymphoid cells was higher than that of patient-matched peripheral blood lymphocytes. That gut mucosal lymphocytes appear to be activated in loco was confirmed by a striking, time-dependent increase in the number of stable E rosettes generated by culturing unstimulated Crohn's disease intestinal lymphoid cells. The responses of lymphocytes from inflamed and normal mucosa to polyclonal mitogens were not only comparable to each other, but to those of corresponding peripheral lymphocytes, as well. Peripheral blood lymphocytes from patients with Crohn's disease showed less proliferation to Bacteroides and lipopolysaccharide antigens than did those from control individuals, but replicated similarly in response to Staphylococcus aureus and the enterobacterial common antigen: In contrast, when cultured with Staphylococcus aureus or with lipopolysaccharides, but mucosal lymphocytes from Crohn's disease proliferated 3-5 times more than did those from normal mucosa, while lymphoid cells from both sources were equally stimulated by Kunin antigen. Overall, this study found no evidence for a defective proliferative capacity of immune competent cells at the gut mucosal level in inflammatory bowel disease.

Colitis↗

PubMed1995

Regulation of superoxide anion generation in bovine alveolar macrophages by bacterial lipopolysaccharide, serum proteins, and modulators of signal transduction.

The respiratory burst of phagocytes in an important leukocyte function which results in generation of oxygen species that are both microbicidal and potentially damaging to host tissues. We investigated regulation of the respiratory burst of alveolar macrophages in response to lipopolysaccharide (LPS) derived from gram-negative bacteria, serum proteins, and several modulators of signal transduction. When employed as a single stimulus, LPS (E. coli 055:B5, 10 ng/ml-1 microgram/ml) was a weak stimulus for generation of superoxide anion (O2-) as compared to the potent effect of the protein kinase C activator, phorbol 12-myristate 13-acetate (PMA; 500 ng/ml). However, when LPS was combined with fetal bovine serum (FBS; 0.4-1.0% vol/vol, equivalent to 128-320 micrograms protein/ml), O2- generation was enhanced approximately two-fold over LPS alone. A chromatographically-derived bovine serum fraction which contained bovine lipopolysaccharide-binding protein (bLBP; 0.25-1.0 microgram/ml) was an effective substitute for FBS at a much lower protein concentration than whole FBS, and a similar synergistic effect with LPS on O2- generation was observed. Stimulation of macrophages for generation of O2- either with LPS alone or with LPS plus serum/serum fraction was suppressed by the protein tyrosine kinase inhibitor heribimycin A (0.2 ng/ml), and the calcium chelator BAPTA (12 microM), but not by modulators of G-proteins, including pertussis toxin (10 ng/ml) and cholera toxin (5 micrograms/ml protein). Essentially complete inhibition of O2- synthesis by herbimycin A and BAPTA occurred in the presence of LPS and the bLBP-containing serum fraction (1 microgram/ml protein), but only partial inhibition (46.7% and 64.1%, respectively) was observed in the presence of LPS plus FBS (256 micrograms/ml protein). These results indicate that when LPS is used as a sole stimulus it induces modest respiratory burst activity. However, when LPS is combined with appropriate serum components, it stimulates alveolar macrophages to generate larger amounts of O2-. Cellular signaling pathways important in stimulation of macrophages by LPS and serum components are protein tyrosine kinase- and Ca(++)-dependent, but do not relay on G-protein-mediated signaling.

Animals↗

PubMed1990

Effect of adherence, cell morphology, and lipopolysaccharide on potassium conductance and passive membrane properties of murine macrophage J774.1 cells.

The effects of adherence, cell morphology, and lipopolysaccharide on electrical membrane properties and on the expression of the inwardly rectifying K conductance in J774.1 cells were investigated. Whole-cell inwardly rectifying K currents (Ki), membrane capacitance (Cm), and membrane potential (Vm) were measured using the patch-clamp technique. Specific Ki conductance (GKi, whole-cell Ki conductance corrected for leak and normalized to membrane capacitance) was measured as a function of time after adherence, and was found to increase almost twofold one day after plating. Membrane potential (Vm) also increased from -42 +/- 4 mV (n = 32) to -58 +/- 2 mV (n = 47) over the same time period. GKi and Vm were correlated with each other; GL (leak conductance normalized to membrane capacitance) and Vm were not. The magnitudes of GKi and Vm 15 min to 2 hr after adherence were unaffected by the presence of 100 microM cycloheximide, but the increase in GKi and Vm that normally occurred between 2 and 8 hr after adherence was abolished by cycloheximide treatment. Membrane properties were analyzed as a function of cell morphology, by dividing cells into three categories ranging from small round cells to large, extremely spread cells. The capacitance of spread cells increased more than twofold within one day after adherence, which indicates that spread cells inserted new membrane. Spread cells had more negative resting membrane potentials than round cells, but GKi and GL were not significantly different. Lipopolysaccharide-(LPS; 1 or 10 micrograms/ml) treated cells showed increased Cm compared to control cells plated for comparable times. In contrast to the effect of adherence, LPS-treated cells exhibited a significantly lower GKi than control cells, indicating that the additional membrane did not have as high a density of functional GKi channels. We conclude that both adherence and LPS treatment increase the total surface membrane area of J774 cells and change the density of Ki channels. In addition, this study demonstrates that membrane area and density of Ki channels can vary independently of one another.

Animals↗

PubMed1979

Degradation of bacterial lipopolysaccharide by gut juice os the snail Helix pomatia.

Lipopolysaccharides from several bacteria were selectively degarded by gut juice of the snail Helix pomatia with extensive loss of anticomplementary activity and changes in the electrophoretic pattern in polyacrylamide gels. The gut juice had little effect on ketodeoxyoctonate content or immunodominant sugars. The lipid A moiety of the lipopolysaccharide appeared to be the main site of attack.

Animals↗

PubMed1994

Change in sensitivity to lipopolysaccharide during the differentiation of human monocytes to macrophages in vitro.

Mononuclear phagocytes in distinct differentiation stages and cultured under different conditions were tested for their sensitivity towards lipopolysaccharide (LPS), using procoagulant activity (PCA) expression and tumor necrosis factor (TNF) production as indices. The response of mature monocyte-derived macrophages differed from that of freshly isolated monocytes 1) by higher levels of constitutive PCA, 2) by responding to approximately 1,000-fold lower concentrations of LPS with PCA and TNF production, and 3) by a faster rise in PCA and TNF production. Due to the high constitutive level of PCA expression, the PCA stimulation index for LPS was low in macrophages when compared with that in monocytes. Thus, during differentiation to macrophages, human monocytes acquire increased sensitivity to LPS (2 orders of magnitude more sensitive than a sensitive turbidimetric Limulus amoebocyte lysate assay). This exquisite sensitivity to LPS is expressed regardless of whether LPS is offered in the presence or absence of lipopolysaccharide binding protein-containing serum. This points to as yet uncharacterized pathways of high affinity interaction between LPS and macrophages.

Blood Coagulation Factors↗

PubMed1982

Action of a polysaccharide fraction of Haemophilus influenzae lipopolysaccharide on macrophage: implication of receptor for mannosyl-polysaccharides.

A polysaccharide fraction (PS) was separated by mild hydrolysis from Haemophilus influenzae lipopolysaccharide. This preparation contained glycosyl-galactosyl, rhamnosyl, glucosaminyl and mannosyl residues (molar ratio: 4-1-1-2-2). It was nontoxic and immunogenic and consisted of at least one stable molecular group (fraction A; MW approximately equal to 10(6)) and an association of aggregated units (fraction B;MW approximately equal to 10(4)). This study evaluated the capacity of phagocytosis and quantitative nitroblue-tetrazolium reduction of mouse macrophages in presence of these polysaccharide fractions. After a 24-h incubation period, PS and fraction A, at 1 mg/ml, increased both phagocytosis and reduction potential of mouse peritoneal macrophages by 100%. In contrast, 1-h incubation with PS or fraction A induced a decrease of 50% in phagocytosis but no modification of NBT reduction. An identical incubation with various sugars showed that only mannosyl polymers could significantly decrease this phagocytic process. As in the case of toxic lipopolysaccharides, macrophages responded to a nontoxic preparation obtained from an endotoxin. We confirmed the role of mannosyl residues in recognition of macrophage binding receptors. Moreover, we suggest that this mannose binding ability was dependent on dose, aggregation state and molecular weight of the preparation.U

Animals↗

PubMedDate not supplied

N-acetylcysteine ameliorates lipopolysaccharide-induced organ damage in conscious rats.

Lipopolysaccharide is strongly associated with septic shock, leading to multiple organ failure. It can activate monocytes and macrophages to release proinflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and nitric oxide (NO). The present experiments were designed to induce endotoxin shock by an intravenous injection of Klebsiella pneumoniae lipopolysaccharide (LPS, 10 mg/kg) in conscious rats. Arterial pressure and heart rate (HR) were continuously monitored for 48 h after LPS administration. N-Acetylcysteine was used to study its effects on organ damage. Biochemical substances were measured to reflect organ functions. Biochemical factors included blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), creatine phosphokinase (CPK), aspartate transferase (GOT), alanine transferase (GPT), TNF-alpha, IL-1 beta, methyl guanidine (MG), and nitrites/nitrates. LPS caused significant increases in blood BUN, Cre, LDH, CPK, GOT, GPT, TNF-alpha, IL-1 beta, MG levels, and HR, as well as a decrease in mean arterial pressure and an elevation of nitrites/nitrates. N-Acetylcysteine suppressed the release of TNF-alpha, IL-1 beta, and MG, but enhanced NO production. These actions ameliorate LPS-induced organ damage in conscious rats. The beneficial effects may suggest a potential chemopreventive effect of this compound in sepsis prevention and treatment.

Acetylcysteine↗

PubMed1992

Bacterial endotoxins as potential antitumor agents. Tumor mass loss in mice treated with bacterial lipopolysaccharides of Shigella dysenteriae serovar 1.

Natural and modified preparations of lipopolysaccharides and lipopolysaccharide-protein complexes isolated from the S- and R-form of Shigella dysenteriae serovar 1 were found to markedly inhibit the initial growth of mouse solid tumors derived from Németh-Kellner lymphoma, Gardner 6C3HED lymphoma, an ill-defined syngeneic lymphoma of DBA mice (Skalsky lymphoma) and LP-2 plasmacytoma. The biopreparations were given intraperitoneally, most frequently at a dose range from 50 to 200 micrograms per mouse; significant inhibitory effects on tumor growth were evidenced even in mice bearing tumors weighing 113 to 507 mg.

Animals↗

PubMed1994

Lipopolysaccharide-induced IgM production is not suppressed by antigen receptor ligation in B cells from some autoimmune strains of mice.

Ligation of surface immunoglobulin on resting or activated nonautoimmune B cells inhibited lipopolysaccharide (LPS)-induced total IgM production. B cells from NZB, (NZB x NZW)F1, and BXSB mice were relatively resistant, but B cells from NZW or MRL/lpr mice were inhibited. The resistance occurs in B cells from young and old NZB mice, and in both resting and activated splenic NZB B cells. Anti-ssDNA responses induced by lipopolysaccharide occur in the presence of antigen-receptor-ligating antibody in NZB, but not in DBA/2, B cells. Antagonism in signaling between the antigen and LPS receptor is not a general B cell hyporesponsiveness, but defects in antagonism specifically between antigen and LPS signaling may be a predisposing factor to autoimmune disease in some autoimmune strains of mice.

Animals↗

PubMed1981

A lipopolysaccharide from Aspergillus flavus conidia.

A lipopolysaccharide was isolated by extraction of Aspergillus flavus conidia with 45% phenol at 68-70 degrees C. Quantitative analysis revealed 7% nucleic acids, 5.5% proteins, 46% polysaccharides and 49% liquids, of which 12% were covalently bound. Glucose, mannose, galactose and fucose were detected as monosaccharide components of the polysaccharide moiety by gas chromatography; palmitic acid, stearic acid, oleic acid, linoleic acid and myristic acid were mainly present in the lipidic fraction. This material differs from the bacterial lipopolysaccharides, both in composition of the polysaccharide moiety and representation of fatty acids in the lipidic fraction.

Aspergillus flavus↗

PubMed2003

Contribution of capsular and lipopolysaccharide antigens to the pathogenesis of Klebsiella pneumoniae respiratory tract infection.

The role of Klebsiella pneumoniae K- and O-polysaccharide antigens was determined in a rat model of lobar pneumonia. The induction of experimental infection in rats by wild-type strain, and its lipopolysaccharide- and capsular polysaccharide-deficient mutants was compared. Though the mutant lacking both antigens (K- O-) induced infection it could not successfully establish itself in the rat lung. It caused only mild infection, as compared to the wild type strain (K+ O+) and the strain lacking CPS alone (K- O+). Besides capsular polysaccharide, the lipopolysaccharide antigen was shown to be an important factor in pathogenesis of K. pneumoniae acute respiratory tract infection.

Animals↗

PubMed2001

Reduced adrenal response to bacterial lipopolysaccharide in interleukin-6-deficient mice.

Administration of bacterial lipopolysaccharide (LPS) in rodents induces the release of pro-inflammatory cytokines [tumor necrosis factor (TNF), interleukin (IL)-1, IL-6] and of ACTH and corticosterone. IL-6 is probably an important cytokine in the interaction between the immune system and the hypothalamus-pituitary-adrenal (HPA) axis, but so far the role of IL-6 in lipopolysaccharide (LPS)-induced HPA activation has not been established unequivocally. We examined the effects of intraperitoneal administration of LPS (range 0.25-2000 pg/mouse) on plasma corticosterone, TNFalpha and IL-1alpha levels in IL-6-deficient (IL-6 -/-) and wildtype control (IL-6 +/+) mice. Plasma corticosterone levels increased within one hour in both mouse strains. The corticosterone response was significantly reduced in IL-6 -/- mice, but no differences in TNFalpha or in IL-1alpha plasma levels were found between the two strains. Next, we studied the involvement of IL-1alpha or TNFalpha in the responses to LPS in IL-6 -/- and IL-6 +/+ mice by infusion of recombinant human IL-1 receptor antagonist (IL-1ra), or by injection of anti-TNFalpha antibodies. Pretreatment with IL-1ra or with anti-TNFalpha did not affect the corticosterone response to LPS, neither in IL-6 -/-, nor in IL-6 +/+ mice. Our data suggest that in the stimulation of the HPA axis by LPS in mice blockade of either IL-1alpha or TNFalpha may be compensated for by other mediators. The reduced adrenal response after LPS administration found in IL-6 -/- mice indicates a distinct role for IL-6 in the activation of the HPA axis by LPS.

Adrenal Glands↗

PubMed2005

Microsomal glutathione S-transferases: selective up-regulation of leukotriene C4 synthase during lipopolysaccharide-induced pyresis.

Cysteinyl-leukotrienes (cys-LTs) are potent smooth muscle contracting agents, which play key roles in inflammatory and allergic diseases. The committed step in cys-LT biosynthesis is catalyzed by leukotriene C(4) synthase (LTC4S) as well as microsomal glutathione S-transferase type 2 (MGST2) and type 3 (MGST3). Here we report that intraperitoneal injections of lipopolysaccharide in rats lead to a strong increase of LTC4S messenger RNA (mRNA) levels after approximately 1 h, particularly in the heart, brain, adrenal glands and liver, without any significant effect on MGST2 and MGST3 mRNA levels. After 6 h, LTC4S mRNA returns to basal levels, concomitant with a 4.9-, 4.0-, 2.9- and 2.3-fold induction of LTC4S protein in brain, heart, liver and adrenal gland, respectively. Hence, challenge with lipopolysaccharide in vivo causes an organ-selective, local priming for leukotriene C(4) synthesis. Moreover, these data suggest that LTC4S and cys-LTs may be involved in acute systemic inflammatory responses such as fever and tachycardia.

Animals↗

PubMed2003

Inhibition of inflammatory responses by ambroxol, a mucolytic agent, in a murine model of acute lung injury induced by lipopolysaccharide.

OBJECTIVE: The aim of this study is to investigate whether ambroxol inhibits inflammatory responses in a murine model of lipopolysaccharide-induced acute lung injury (ALI). METHODS: Mice (n=295) were first intratracheally instilled with lipopolysaccharide (LPS) to induce ALI and then received an intraperitoneal (i.p.) injection of either normal saline (NS), ambroxol (30 or 90 mg/kg per day) or dexamethasone (2.5 or 5 mg/kg per day) for 7 days. Metabolism (n=10, each), lung morphology (n=5, each) and wet-to-dry lung weight ratio (n=10, each) were studied. The levels of tumor necrosis factor (TNF-alpha), interleukin-6 (IL-6) and transforming growth factor (TGF-beta1) and the protein concentration (n=5 or 7, each) in bronchoalveolar lavage (BAL) were measured. RESULTS: Mice with LPS-induced ALI that were treated with ambroxol at a dosage of 90 mg/kg per day significantly gained weight compared to the control and dexamethasone-treated groups. Ambroxol and dexamethasone significantly reduced the lung hemorrhage, edema, exudation, neutrophil infiltration and total lung injury histology score at 24 and 48 h. In addition, ambroxol and dexamethasone significantly attenuated the lung wet-to-dry weight ratio at 24 and 48 h (p<0.05). Compared to the control group, TNF-alpha, IL-6 and TGF-beta1 levels in the BAL in both ambroxol- and dexamethasone-treated groups were significantly reduced at 24 and 48 h. The protein in BAL, an index of vascular permeability, was also significantly decreased in the ambroxol- and dexamethasone-treated groups (p<0.05). CONCLUSION: Ambroxol inhibited proinflammatory cytokines, reduced lung inflammation and accelerated recovery from LPS-induced ALI.

Ambroxol↗

PubMed2005

Effects of lipopolysaccharides from gram-negative bacteria on the level of thiols in blood platelets.

Lipopolysaccharide (endotoxin, LPS) activates blood platelets and stimulates generation of free radicals in these cells. The mechanism of platelet activation induced by LPS is not known. The aim of the present study was to examine how glutathione (GSH) and other thiol-containing compounds are involved in the oxidative stress in blood platelets caused by LPS. The HPLC technique has been used on the analysis of non-protein thiols from human blood platelets treated with lipopolysaccharides of different gram-negative bacteria (Proteus mirabilis, Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa). Our results show that LPSs caused an increase (about 10%) of the level of reduced glutathione (GSH) and other nonprotein thiols such as cysteine (CSH) and cysteinylglycine (CGSH), whereas the total pool of these compounds was almost unchanged. LPS may react directly with thiols, since after incubation of LPSs with glutathione alone (in reduced form) we observed a distinct decrease of the level of platelet GSH.

Blood Platelets↗

PubMed2003

Clinical value of lipopolysaccharide-binding protein (LBP) determinations in acute pancreatitis.

BACKGROUND: Lipopolysaccharide-binding protein (LBP) is a class 1 acute-phase protein that binds and transfers bacterial lipopolysaccharide (LPS). This study investigated the clinical value of measuring LBP for stratifying biochemical severity in acute pancreatitis by using a recently developed fully automated assay technique. PATIENTS AND METHODS: We studied 71 patients with acute pancreatitis of whom 41 presented with a necrotizing course. Necrotizing pancreatitis was associated with pancreatic infections in 21 patients and with multiorgan dysfunction syndrome (MODS) in 18 patients. Serum LBP was measured for 14 days by a fully automated immunoassay and CRP was assessed on a daily routine basis. RESULTS: The relative quantitative systemic release of LBP was lower than that observed for CRP; however, the two parameters revealed similar dynamics, with a maximum increase in acute pancreatitis around the fourth day after onset of symptoms. As observed for CRP, LBP was significantly higher in patients who developed complications such as necrosis, pancreatic infections, single or combined MODS than in those who did not. Multiple regression analysis revealed that pulmonary failure and MODS were independent variables associated with enhanced LBP release, while the development of necrosis, pancreatic infections and MODS were the corresponding variables for increased CRP levels. CONCLUSIONS: Systemic LBP concentrations are significantly elevated in acute pancreatitis and closely correlate with overall disease severity. However, compared with CRP, LBP does not contribute to an improved severity stratification in acute pancreatitis.

Acute Disease↗

PubMed2000

The role of tumor necrosis factor (TNF) in the febrile and metabolic responses of rats to intraperitoneal injection of a high dose of lipopolysaccharide.

The role of tumor necrosis factor (TNF) in the febrile and metabolic responses of rats to intraperitoneal injection of a high dose of lipopolysaccharide Injection of a high dose of lipopolysaccharide (LPS) induces a septic-shock-like state, which can be accompanied by phases of hypothermia and phases of fever. In the present study we monitored body core temperature and locomotor activity, both by remote radiotelemetry, as well as changes in food intake, body mass and water intake for 3 days after an intraperitoneal (i.p.) injection of a high dose of LPS (5 mg/kg) along with sterile 0.9% saline or a neutralizing form of the soluble tumor necrosis factor (TNF) type 1 receptor (referred to as TNF-binding protein, TNF bp). Intraperitoneal injection of LPS rapidly induced high concentrations of TNF in the plasma and peritoneal lavage fluid. TNF was undetectable in the plasma and peritoneal lavage fluid of animals co-injected with LPS and TNF bp, implying neutralization of peripheral bioactive TNF. Administration of LPS induced hypothermia by about 1.5 degrees C, which lasted for 5 h after injection. During the light-time periods of days 2 and 3 after injection, the rats developed a robust fever. Treatment with TNF bp resulted in a faster recovery from the LPS-induced hypothermia so that the rats developed a pronounced fever on the day of injection. Locomotor activity during night-time periods was suppressed in LPS-treated animals. The LPS-induced depression of night-time activity was not antagonized by co-injection of TNF bp. On day 1 after the injection of LPS, food intake reduced to virtually zero, water intake fell to about 30% of the control value and body mass dropped by 25 g (about 10% of total body mass). With the exception of body mass, these variables recovered slowly during days 2 and 3 after LPS injection, but did not reach the control values. The LPS-induced decreases in food intake, body mass and water intake were significantly attenuated by the treatment with TNF bp. These results confirm that TNF contributes significantly to the rats' responses to intraperitoneal injection of a high dose of LPS. The fact that treatment with TNF bp accelerated and improved the rats' ability to develop a febrile response supports the view that the fever is beneficial, since all other metabolic responses measured in this study were normalized more effectively in those rats that developed a faster and more pronounced increase in body temperature.

Animals↗