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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A "new" polyclonal activator of human peripheral blood B cells, formaldehyde-fixed Salmonella paratyphi B, is described. This bacterium does not stimulate cell proliferation as measured by incorporation of tritiated thymidine but does stimulate a subpopulation of B cells to secrete large amounts of IgM, IgG, and IgA in 7-day cell cultures. The immunoglobulins (Ig) produced by cells responding to S. paratyphi B are not specific antibodies against the bacterial antigens. In comparison with other B cell activators (pokeweed mitogen, Staphylococcus aureus Cowan I, and lipopolysaccharide), S. paratyphi B stimulation produced greater amounts of IgM but less IgG than pokeweed mitogen (PWM) or S. aureus Cowan I; lipopolysaccharide failed to stimulate significant Ig production on day 7 in most cases. In addition, the response to S. paratyphi apparently did not require T cell collaboration. These results suggest that the B cell subpopulation(s) responding to S. paratyphi B may be more differentiated B cells than those responding to either PWM or S. aureus Cowan I. Peripheral blood mononuclear cells from five patients with common variable immunodeficiency without evidence of abnormal suppressor T cells or monocytes failed to respond to S. paratyphi B, whereas cells from two of the same patients responded well to S. aureus Cowan I and partially to PWM. Thus, S. paratyphi B appears to be superior to other B cell activators for studies of B cell function in normal and abnormal states.
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PMID:Polyclonal activation of human peripheral blood B lymphocytes by formaldehyde-fixed Salmonella paratyphi B. I. Immunoglobulin production without DNA synthesis. 697 34

A recombinant 23-kDa amino-terminal fragment of human bactericidal/permeability-increasing protein (rBPI23), a potent lipopolysaccharide (LPS)-binding/neutralizing protein, was used as a probe to assess the role of endotoxin in the acute inflammatory responses elicited by gram-negative bacteria in rat subcutaneous air pouches. In initial experiments, rBPI23 prevented the Escherichia coli O111:B4 LPS-induced accumulation of polymorphonuclear leukocytes (PMN), tumor necrosis factor alpha (TNF-alpha), and nitrite (a stable end product of nitric oxide formation) in exudate fluids. Significant inhibition of TNF-alpha production was still evident when rBPI23 treatment was delayed for 30 min after LPS instillation. In subsequent experiments, rBPI23 also prevented the nitrite and early (2-h) TNF-alpha accumulation induced by three different strains of formaldehyde-killed gram-negative bacteria (E. coli O7:K1, E. coli O111:B4, and Pseudomonas aeruginosa 12.4.4) but did not inhibit the PMN or late (6-h) TNF-alpha accumulation induced by these bacteria. As with LPS challenge, a significant inhibition of early TNF-alpha production was still evident when rBPI23 treatment was delayed for 30 to 60 min after instillation of killed bacteria. The results indicate that in this experimental model the NO and early TNF-alpha responses to gram-negative bacterial challenge are mediated predominantly by endotoxin, whereas the PMN and late TNF-alpha responses may be mediated by other bacterial components. Moreover, the results indicate that rBPI23 can inhibit the bacterially induced production of certain potentially harmful mediators (TNF-alpha and NO) without entirely blocking the host defense, i.e., PMN response, against the bacteria.
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PMID:Role of endotoxin in acute inflammation induced by gram-negative bacteria: specific inhibition of lipopolysaccharide-mediated responses with an amino-terminal fragment of bactericidal/permeability-increasing protein. 780 73

We have investigated the interaction of Salmonella minnesota R595 lipopolysaccharide (ReLPS) depleted of Ca2+ and Mg2+ with both Kupffer and endothelial liver cells under serum-free conditions. Specific and saturable binding levels of 125I-ReLPS were similar in both types of cells with respect to divalent cation independence, susceptibility to proteases, and concanavalin A inhibition. By using partial structures of ReLPS, it was demonstrated that acidic 3-deoxy-D-manno-octulosonic acid residues and phosphoryl groups on lipid A are of primary importance in ReLPS binding. The role of ionic interactions in LPS recognition by the cells was further confirmed by susceptibility of the binding to competitive inhibition by polyanions. Both ReLPS and ReLPS partial structures inhibited the specific cellular binding of acetylated low-density lipoprotein (Ac-LDL) by Kupffer cells and Ac-LDL- and formaldehyde-treated albumin by endothelial cells whose cellular accumulation is mediated by a different type(s) of scavenger receptor(s). In contrast, 125I-ReLPS binding to Kupffer and endothelial cells was not competed by Ac-LDL or formaldehyde-treated albumin. Our results indicate the scavenger pathway of LPS uptake by Kupffer and endothelial cells and the primary role of LPS anionic properties in this process.
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PMID:Scavenger receptor pathway for lipopolysaccharide binding to Kupffer and endothelial liver cells in vitro. 786 58

In view of the controversy concerning the expression of chlamydial lipopolysaccharide (LPS) in the eukaryotic host cell, the presence of this molecule was examined in three cell types which were experimentally infected with Chlamydia trachomatis serotype E. LPS was detected in the McCoy cell line, human endometrial epithelium and human amniotic epithelium with two monoclonal antibodies. The appearance and distribution of LPS at the host cell surface during the chlamydial developmental cycle and its transmission to neighbouring cells were examined by immunofluorescence microscopy after air drying of the host cells. LPS distribution was not uniform; it was first observed on regions of the cell surface in close proximity to the chlamydial endosome (inclusion). Soon after, the antigen was also detected at points of contact with neighbouring uninfected cells. Immunofluorescent plaques of host cells contaminated with LPS were thus formed in the vicinity of infected cells. These plaques increased in size over 2 d before becoming smaller as host cell lysis occurred. The major outer-membrane protein (MOMP) was not visualized on the host cell surface after air drying. No cell-surface LPS antigen was observed in live cells or those fixed in formaldehyde without air drying. Conventional methanol fixation and immunolocalization of LPS and MOMP in parallel infected cultures stained these antigens within inclusions in the expected fashion. Radio-immunoassays were used to quantify LPS in confluent McCoy cell monolayers during the chlamydial developmental cycle. Cell-surface-associated and inclusion-associated LPS, measured by direct binding of 125I-labelled anti-LPS monoclonal antibodies to air-dried or methanol-fixed monolayers respectively, increased for up to 3 d then declined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipopolysaccharide in cells infected by Chlamydia trachomatis. 792 Dec 50

Malonaldehyde (MDA), a product of lipid peroxidation, is a presumptive marker for the development of oxidative stress in tissues and plasmas. In this study we report the photodiode array detection of the 2,4-dinitrophenylhydrazine (DNPH) derivatives of MDA using HPLC. Oxidative stress was produced by injecting (i.p.) bacterial lipopolysaccharide (LPS) into rats at a dose of 100 micrograms/kg, or i.v. into rabbits (1 microgram/kg), or added to freshly drawn human blood (200 ng/ml). Blood was collected at several time points up to 5 h, centrifuged, and equal volumes of 20% TCA were used to precipitate proteins from the plasma. The supernatants were derivatized with DNPH, and the aldehyde-DNPHs were extracted with pentane. After evaporation, aliquots of 10 microliters in acetonitrile were injected onto a Beckman Ultrasphere C18 (3 microns) column, chromatographed with an acetonitrile-water-acetic acid gradient mobile phase and scanned using Waters 996 photodiode array detector. Peak identification and homogeneity was determined by comparing the experimental peaks and UV scans with those of authentic standards. A significant increase in the DNPH derivative of malonaldehyde (MDA-DNPH), but not of the other aldehyde-DNPH derivatives of formaldehyde (FDA), acetaldehyde (ADA), acetone and propionaldehyde (PDA) was seen over the first hour after LPS administration in anesthetized rats, while in conscious rabbits this trend lasted up to 3 h. The retention times as well as the UV scans of the derivatized aldehydes matched the authentic standards. Thus, photodiode array detection has proved valuable in establishing this HPLC method for estimating oxidative stress. This technique could accurately measure pmol amounts of MDA-DNPH indicating the usefulness of photodiode array detection method for estimating small changes in the oxidative stress.
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PMID:High-performance liquid chromatographic peak identification of 2,4-dinitrophenylhydrazine derivatives of lipid peroxidation aldehydes by photodiode array detection. 954 33

We have adapted the purpald assay (M. S. Quesenberry and Y. C. Lee, Anal. Biochem. 234, 50-55, 1996) to quantify lipopolysaccharide (LPS) content in solution in 96-well microtiter plates at room temperature. This method employs the oxidation of unsubstituted terminal vicinal glycol groups in 2-keto-3-deoxyoctonate (Kdo) and l-(or d-)glycero-d-manno-heptose of LPS molecules by periodate to release formaldehyde. The formaldehyde is quantified at 550 nm (or 530-570 nm) by reacting with purpald reagent followed by oxidation with NaIO4. The sensitivity of the purpald assay is comparable to that of the Kdo assay for LPS determination. However, the purpald assay is superior to the Kdo assay because: (i) No acid hydrolysis of the samples and no boiling in the assay process are required; thus, it can be directly carried out with microtiter plates for a large number of samples at room temperature. (ii) The purpald assay can detect many types of LPS from various bacteria since LPS contains Kdo and heptose which possess unsubstituted terminal vicinal glycol in its structure, while the Kdo assay cannot detect LPS from certain bacteria (e.g., Haemophilus influenzae, Bordetella pertussis, and Vibrio cholerae) due to substitution at the C-4 and C-5 positions of Kdo.
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PMID:Quantification of bacterial lipopolysaccharides by the purpald assay: measuring formaldehyde generated from 2-keto-3-deoxyoctonate and heptose at the inner core by periodate oxidation. 991 68

The mechanism of elimination of blood-borne Vibrio salmonicida lipopolysaccharide (LPS) from Atlantic cod (Gadus morhua L.) was studied. The anatomical distribution of LPS was determined using both morphological and radiotracing methods. Immunohistochemistry performed on tissue specimens after injection of LPS disclosed that the endocardial endothelial cells (EECs) represented the cellular site of uptake in heart. Co-injection of trace amounts of [(125)I]LPS together with excess amounts of formaldehyde-treated albumin (FSA), a ligand for the scavenger receptor, significantly inhibited the accumulation of the radiotracer in heart only. Studies on purified monolayer cultures of atrial EECs showed that fluorescein-labelled LPS was taken up in structures reminiscent of endosomal/lysosomal vesicles. Incubation of cultures with [(125)I]LPS together with excess amounts of FSA, fucoidan and dextran sulphate, molecules known to compete for endocytosis via the scavenger receptor, reduced uptake of the probe by 80 %. Mannan, a ligand for the mannose receptor, did not compete for uptake. Kinetic studies on the uptake and degradation of [(125)I]LPS in cultured atrial endocardial cells revealed no degradation after 48 h of culture. In conclusion, we have shown that the EECs of cod remove V. salmonicida LPS from the circulation by scavenger-receptor-mediated endocytosis.
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PMID:Scavenger-receptor-mediated endocytosis of lipopolysaccharide in Atlantic cod (Gadus morhua L.). 1180 80

Up to now there is no treatment for staphylococcal toxic shock syndrome, a disease mainly induced by toxic shock syndrome toxin-1(TSST-1). There is great demand in finding means to control the disease, one of them is the development of an effective and safe vaccine against TSST-1. In this study we constructed a series of vaccine candidates and investigated their biological activity, toxicity, and potential to invoke an immune response. TSST-1 was isolated from Stahylococcus aureus supernatants and recombinantly expressed as a N-terminal 6x histidine-tagged protein in Escherichia coli. In order to obtain molecules with minimal toxicity we constructed single mutants (G31R and H135A) and one double mutant (G31R/H135A) with both residues exchanged. We also detoxified native TSST-1 isolated from S. aureus, and recombinantly expressed TSST-1 by treatment with formaldehyde. Functional activity of native and recombinant TSST-1 and grade of inocuity of mutants and toxoids was determined by investigating mitogenity, T-cell activation, and cytokine release upon stimulation of human mononuclear cells with the vaccine candidates. All substances were tested in a rabbit immunization study. After primary immunization and three additional boosts all vaccinated animals developed antibody titers against TSST-1 and were protected against challenge with a lethal doses of superantigen potentiated with lipopolysaccharide.
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PMID:Double mutant and formaldehyde inactivated TSST-1 as vaccine candidates for TSST-1-induced toxic shock syndrome. 1181 53

The potential of organic dust to induce inflammation in vitro can be viewed as a crude measure of the total biologically active compounds in a dust sample. The purpose of this study was to further develop an in vitro screening method for evaluation of potential hazard related to low doses of dust exposure using two monocytic cell lines (U937 and THP-1). Dust was obtained from schools in Copenhagen. U937 and THP-1 cells were stimulated with dust for 24 h and interleukin-8 secretion was measured. The initial slopes of the dose-response curves were used to calculate the inflammatory potential, or potency factor (PF), of the samples. In characterization of the method, lipopolysaccharide from Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Salmonella enteritidis were tested together with three glucans, nickel sulfate (NiSO(4)), methyl methacrylate (MMA), formaldehyde, and four surfactants. The PF values of LPSs in both monocytic assays ranked as follows: S. enteritidis> E. coli>K. pneumoniae/P. aeruginosa. The PF values of NiSO(4), MMA, formaldehyde, and the surfactants were zero or below. Using the THP-1 cell line, the PF values of dust samples were 30 times higher than when using the U937 cell line, and 7 times higher than when using the lung epithelial cell line (A549). The high sensitivity of the THP-1 bioassay makes it potentially useful as a screening tool for hazard evaluation of dust from, e.g., the indoor environment.
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PMID:Interleukin-8 secretion from monocytic cell lines for evaluation of the inflammatory potential of organic dust. 1205 97

It is suspected that exposure to low levels of formaldehyde induces or aggravates airway inflammation mediated by immunological and neurological reactions. To clarify the effect of this exposure on allergic inflammatory responses, we exposed female C3H/He mice to 0, 80, 400, or 2000ppb formaldehyde for 12 weeks. When mice were immunized with ovalbumin (OVA) and then exposed to formaldehyde, the numbers of total bronchoalveolar lavage cells, macrophages, and eosinophils in the mice exposed to 2000ppb formaldehyde were significantly increased compared to 0ppb controls. However, the production of interleukin-1beta from bronchoalveolar lavage fluid of these mice decreased significantly. Immunization with OVA significantly increased the production of nerve growth factor, but exposure to 80 and 400ppb formaldehyde significantly reduced the nerve growth factor levels in bronchoalveolar lavage fluid of the immunized mice. In in vitro study, markedly increased lipopolysaccharide-stimulated interferon-gamma production in culture supernatants of spleen cells from 2000ppb formaldehyde-exposed, nonimmunized mice, and significantly increased OVA-stimulated monocyte chemoattractant protein-1 production in culture supernatants of spleen cells from 400 and 2000ppb formaldehyde-exposed, immunized mice were observed. Exposure to 400ppb formaldehyde induced significant decreases in anti-OVA IgG1 and IgG3 antibody productions in plasma, whereas anti-OVA IgE antibody production was not affected. In addition, the levels of nerve growth factor in plasma of 80 and 400ppb formaldehyde-exposed, immunized mice significantly decreased compared to 0ppb control, immunized mice. These results provide the first experimental evidence that low levels of long-term formaldehyde inhalation can induce differential immunogenic and neurogenic responses in allergic mice.
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PMID:Differential immunogenic and neurogenic inflammatory responses in an allergic mouse model exposed to low levels of formaldehyde. 1500 29


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