Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bradykinin (BK) and Tyr8-BK induced graded rat paw edema with EC50 values of 1.9 and 1.1 nmol/paw, while des-Arg9-BK (DABK, up to 300 nmol/paw) was marginally effective. Tyr8-BK, but not DABK, also caused a dose-related increase in mouse paw edema, with an EC50 of 1.3 nmol/paw. The response to Tyr8-BK (10 nmol/paw) in rat paw edema was antagonized by B2 receptor antagonists (HOE-140 or NPC 17731, 30 nmol/paw) but not by the B1 antagonist des-Arg9[Leu8]BK (DALBK, 100 nmol/paw). Daily intraplantar injections of Tyr8-BK (10 nmol/paw) for 7 days caused progressive desensitization (D) of edema in sham-operated and adrenalectomized Wistar rats. DABK (100 nmol/paw) caused marked paw edema in D paws from both groups, which was inhibited by DALBK (100 nmol/paw) and by dexamethasone (0.5mg/kg, s.c.). Systemic injection of lipopolysaccharide (10 micrograms/mouse, 24 h prior) potentiated the first and second phases of Formalin-induced pain but had no effect on paw edema. Coinjection of DABK (2-22 nmol/paw) with low doses of Formalin in lipopolysaccharide-treated mice, which had no effect on naive animals, dose dependently potentiated both phases of Formalin-induced pain but did not modify paw edema. These effects were antagonized by DALBK with ID50 values of 21.9 (first phase) and 64.1 (second phase) nmol/paw. Thus, both progressive desensitization of B2 receptors and systemic treatment with lipopolysaccharide induce a glucocorticoid-sensitive upregulation of B1 receptors mediating paw edema in the rat and Formalin-induced nociception in mice. These results suggest that induction of upregulation of B1 receptors may play important roles in controlling inflammatory processes and hyperalgesia.
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PMID:Expression of B1 kinin receptors mediating paw edema and formalin-induced nociception. Modulation by glucocorticoids. 884 14

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

Case reports and serological work have raised the possibility that chlamydias can infect the placenta and thus harm the fetus. We investigated the involvement of Chlamydia in a series of 195 unselected cases of spontaneous abortion or miscarriage. Formalin-fixed placental tissues from all cases were examined immunohistochemically, for the presence of chlamydial lipopolysaccharide, as well as histopathologically. A serum sample was collected from 187 of the patients for detection of anti-chlamydial antibodies by microimmunofluorescence. All placental sections were negative for chlamydial antigen. Serological findings indicated that 8 patients had been in contact with C. trachomatis, 15 patients with C. pneumoniae, and none with C. psittaci. A few cases of perivillitis or intervillitis were detected, but none exhibited the intracytoplasmic inclusions typical of C. psittaci. Although these results are negative a search for Chlamydia in abortion materials should be encouraged.
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PMID:No association of Chlamydia with abortion. 1047 59

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

The purpose of this study was to compare the immunoreactivity in canine renal tissues stained with antisera specific for 3 leptospiral antigens and those processed with traditional staining methods. In addition, immunoglobulin staining was done on tissues with immunoreactivity to leptospiral antigens. Formalin-fixed renal sections from 12 dogs with chronic interstitial nephritis suspected or proven to have leptospirosis (6 dogs with silver-stained leptospires and 6 dogs in which silver-stained leptospires were not detected) were used. Antibodies consisted of a monoclonal antibody to Leptospira kirschneri serovar grippotyphosa lipopolysaccharide (LPS) and 2 polyclonal antibodies to outer membrane proteins, including OmpL1, a leptospiral porin, and LipL41, an outer membrane lipoprotein. The murine monoclonal antisera against LPS (F71C2-1) had the most abundant and consistent immunoreactivity. Immunoreactive areas were present in 6 of 6 sections positive by silver staining and included extracellular granular debris in intertubular areas, debris in macrophages, organisms in tubular lumina, and cytoplasmic granules in tubular epithelia. Antisera with specificity for the outer membrane proteins OmpL1 and LipL41 detected only intact organisms in tubular lumina. Immunoreactivity to OmpL1 (polyclonal 338) occurred in 4 of 5 sections positive by silver staining, but immunoreactivity to LipL41 (polyclonal 813) occurred in only 1 of 6 silver-positive sections. Each of the kidney sections in which leptospiral antigens were detected by immunohistochemistry also was positive by silver staining. Sections negative by silver staining were also negative by immunostaining. Although immunohistochemistry did not enhance sensitivity, amplification of signal by secondary antibody and hematoxylin counterstaining improved the ease of diagnosis and allowed better evaluation of tissue morphology than did silver staining methods. IgG was the most abundant immunoglobulin. IgG immunoreactivity occurred predominantly in plasma cells within interstitial infiltrates. Interstitial infiltrates contained abundant immunoreactivity to LPS, but immunoreactivity to OmpL1 and LipL41 was not noted.
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PMID:An improved immunohistochemical diagnostic technique for canine leptospirosis using antileptospiral antibodies on renal tissue. 1268 Jun 39

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

Interleukin-18 (IL-18) is an 18-kDa cytokine produced by lipopolysaccharide (LPS)-activated macrophages or Kupffer cells. In addition, IL-18 is also produced by many different types of cells and tissues, including epidermal keratinocytes, the adrenal cortex, and the brain. IL-18 acts on the immune system to increase IFN-gamma production from T and NK cells to enhance NK cell cytotoxicity and to activate Th1 cell proliferation. It is considered that the tissue expression of cytokines and cell adhesion molecules such as ICAM-1 are common in graft-versus-host disease (GVHD). Recent evidence suggests that IL-18 is a cytokine relevant in the pathogenesis of GVHD. Despite the potential importance of IL-18 in GVHD, the distribution of IL-18 production in cutaneous GVHD has not been fully investigated. In this study, the expression of IL-18 in the cutaneous GVHD was investigated. Formalin-fixed, paraffin-embedded tissue sections were obtained, and immunohistochemical analysis was performed to detect IL-18 and ICAM-1 expression according to the acute and chronic GVHD. Immunohistochemical analysis confirmed the enhanced IL-18 expression levels in the early stage (grade 1) of acute GVHD and the late stage (sclerodermoid) of chronic GVHD compared to the other stages. In contrast, the ICAM-1 expression level was constant at all stages. Our findings indicate that IL-18 is a significant pathogenic indicator in cutaneous GVHD, and the tissue expression of IL-18 seems to be associated with the pathogenesis of acute and chronic GVHD.
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PMID:Increased expression of IL-18 in cutaneous graft-versus-host disease. 1532 98


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