Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The cell cycle kinetics of lipopolysaccharide (LPS)-stimulated spleen cells were measured by acridine orange (AO) staining and flow cytometry. We have devised a computer model to predict the proportions of cells in each cell cycle phase using iteratively varied parameters. The optimum fit between the predicted and observed proportions of cells in various phases of the cell cycle was determined using the minimum sigma chi 2. The model then correlates the variability of intermitotic phase time with the proportion of genomic DNA available for immunoglobulin (Ig) switch region (S mu) rearrangement. This analysis predicts that rearrangements at S mu are cell cycle-dependent events which occur during the first S phase after LPS activation. Molecular analysis of this system confirms these predictions.
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PMID:Cell cycle kinetics model of LPS-stimulated spleen cells correlates switch region rearrangements with S phase. 381 34

To gain insight into the function of cell surface IgM (sIgM) and IgD (sIgD), the expression of these markers on B lymphocytes was quantitated during activation and progression through the cell cycle. Specifically, analysis and correlation of changes in cell cycle state, sIgM and sIgD expression and cell size following exposure of murine B cells to mitogenic levels of lipopolysaccharide and dextran sulfate is reported. As assessed by flow cytometric acridine orange analysis, a large proportion of normal splenic B cells respond within 48 h of exposure to these mitogens by entry into the cell cycle. This response is accompanied by an increase in cell size as determined by flow cytometric "time of flight" measurement. Flow cytometric immunofluorescence analysis reveals a simultaneous alteration in sIg expression. Specifically, cells leaving G0 and transiting G1 increase in diameter from 5 microns to 6 microns and lose greater than 80% of sIgD while sIgM remains constant. Progression through the remainder of the cell cycle is accompanied by a further increase in mean cell diameter to approximately 12 microns while sIgM and sIgD levels remain at G1 levels. The abrupt loss of sIgD as cells transit G1 suggests that an active process mediates this decrease.
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PMID:B lymphocyte activation: entry into cell cycle is accompanied by decreased expression of IgD but not IgM. 660 Oct 15

We report analyses of the effect of anti-Fab antibodies on plasma membrane potential of mouse B lymphocytes. Results indicate that divalent fragments of anti-Fab antibodies mitogenic for B cells stimulate membrane depolarization detectable by cytofluorometric analysis of 3,3'-dipentyloxacarbocyanine iodide-stained cells. Depolarization is detectable within 5 min of exposure to ligand and maximal within 1 h of exposure when greater than or equal to 80% of splenic B cells exhibit decreased membrane potential. The ineffectiveness of monovalent Fab antibody fragments in inducing this event suggests that receptor immunoglobulin cross-linking is essential. Frequencies of cells induced to enter cell cycle, as assessed by acridine orange cell cycle analysis, are equal to those induced to depolarize by lipopolysaccharide plus dextran sulfate or anti-Fab, which suggests a relationship between these events. However, membrane depolarization is itself an insufficient signal to promote subsequent thymidine uptake, as evidenced by the fact that doses of anti-Fab that are suboptimal for thymidine uptake induce maximal depolarization. These results suggest that cross-linking of surface immunoglobulin on B cells may provide an initial signal for activation but is itself insufficient to drive B cell proliferation.
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PMID:B cell activation. I. Anti-immunoglobulin-induced receptor cross-linking results in a decrease in the plasma membrane potential of murine B lymphocytes. 660 4

Here we report analysis and correlation of changes in cell size and cycle state resulting from exposure of murine B lymphocytes to the mitogens lipopolysaccharide (LPS) and dextran sulfate (DxSO4). Cell cycle changes are assessed by flow cytofluorometric analysis of acridine orange stained cells. Cell diameters are determined by flow cytometric analysis of the pulse-width (time of flight) of the axial light extinction signal. Results indicate that within 12 h of exposure of B cell populations to these mitogens, cells displaying increased diameter and containing increased RNA can be detected. Under these conditions, increased RNA content is considered indicative of G0 to G1 transition or entry into cell cycle (Darzynkiewicz et al., 1976). Progressive increases in cell size and transition through G1, S, G2, and M occur in parallel during 48 h of culture with mitogens. Sorting of cells based upon size followed by cell cycle analysis reveals a direct correlation between cell size and cycle phase. Specifically, cells 4.5-5.5 microns in diameter are in primarily G0. Cells 5.5-7.0 microns in diameter are in early G1. Populations of cells 7.0-10 microns in diameter are comprised of late G1 and S phase cells. Populations of cells 10-12 microns in diameter consist of S, G2, and M phase cells. The importance of this correlation is discussed in view of needs to more rigorously define B cell populations for investigations of biochemical events of and accessory cell requirements for activation of B lymphocytes.
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PMID:Sorting of B lymphoblasts based upon cell diameter provides cell populations enriched in different stages of cell cycle. 660 56

By using the intravital microscope equipped with digital imaging processor, we investigated the granulocyte-mediated oxidative burst during the endotoxin-induced microvascular derangement in rat mesentery. The leukocyte behavior after the injection of acridine orange was detected by using a silicon-intensified target camera, the erythrocyte velocity was measured by using a high-speed video camera system, and the luminol-dependent photoemission was visualized by an ultrasensitive photon-counting camera in lipopolysaccharide (LPS)-treated microvascular beds. At 60 min after the LPS administration, a significant leakage of FITC-labeled albumin was observed along mesenteric venules under a fluorescence microscopy. The number of sticking leukocytes increased in association with the decrease in erythrocyte velocity after starting the LPS infusion. The luminol-dependent chemiluminescence in microvascular beds gradually increased over that recorded prior to LPS exposure and was fourfold higher 60 min after the start of LPS infusion. The distribution of the photoemission clearly corresponded to the venular endothelium, to which leukocytes adhered. In blood samples taken from the mesenteric vein at 60 min after the LPS administration, a decrease in the number of granulocytes and increases of total and individual chemiluminescence activities were observed. These results suggest that LPS induces oxidative burst from granulocytes on the venular endothelium. Cetraxate, an inhibitor of proteases including plasmin, significantly inhibited the leukocyte activation and prevented alterations in microvascular hemodynamics induced by LPS in vivo, whereas it had no effect on the LPS-induced oxyradical generation from adherent leukocytes in vitro. The present study demonstrates that proteases such as plasmin may play an important role in the pathogenesis of endotoxin-induced microvascular disturbances.
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PMID:Oxyradical generation from leukocytes during endotoxin-induced microcirculatory disturbance in rat mesentery--attenuating effect of cetraxate. 851 81

P-selectin is one of the adhesion molecules involved in leukocyte rolling during an inflammatory reaction. The aim of this study was to examine the role of P-selectin in leukocyte-endothelial interactions in retinal microcirculation during ocular inflammation, known as endotoxin-induced uveitis (EIU), in vivo. EIU was induced in Lewis rats by footpad injection of lipopolysaccharide (LPS). At the time of LPS treatment or 12 h later, anti-rat P-selectin mAb (ARP) was injected intravenously, and its effect on leukocyte behavior in the retina was studied after intravital staining with acridine orange using a scanning laser ophthalmoscope. P-selectin gene expression in the retina was also studied by a semiquantitative polymerase chain reaction (PCR) method. Administration of ARP at the time of LPS treatment significantly reduced the number of rolling leukocytes at 6 and 12 h by 68% (P < 0.05) and 83% (P < 0.01), respectively, and the number of cells infiltrating the vitreous at 48 h by 61% (P < 0.05). Interestingly, ARP significantly inhibited the vasodilation observed during EIU. In contrast, delayed administration of ARP blocked neither cellular infiltration nor vasodilation. P-selectin gene expression was upregulated during the course of EIU. In conclusion, P-selectin may significantly contribute to the development of inflammation in the early stage of endotoxin-induced ocular inflammation.
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PMID:In vivo neutralization of P-selectin inhibits leukocyte-endothelial interactions in retinal microcirculation during ocular inflammation. 965 23

Several recent Escherichia coli O157:H7 outbreaks associated with both drinking and recreational water raise concerns about waterborne illness caused by this pathogen. The survival characteristics of a mixture of five nalidixic acid-resistant E. coli O157:H7 strains (10(3) CFU/ml) in filtered and autoclaved municipal water, in reservoir water, and in water from two recreational lakes were determined for a period of 91 days at 8, 15 or 25 degrees C. Greatest survival was in filtered autoclaved municipal water and least in lake water. Regardless of the water source, survival was greatest at 8 degrees C and least at 25 degrees C. E. coli O157:H7 populations decreased by 1 to 2 log10 by 91 days at 8 degrees C, whereas the pathogen was not detectable (> or 3 = log10 decrease) within 49 to 84 days at 25 degrees C in three of the four water sources. SDS-PAGE of surface antigens of surviving cells revealed that there was no major alteration in lipopolysaccharide pattern, but outer membrane protein composition did change. These studies indicate that E. coli O157:H7 is a hardy pathogen that can survive for long periods of time in water, especially at cold temperatures. However, direct viable counts of E. coli O157:H7 determined by acridine orange staining remained essentially the same for 12 weeks at 25 degrees C, whereas viable counts on tryptic soy agar plates decreased to undetectable levels within 12 weeks. Results suggest that E. coli O157:H7 can enter a viable but nonculturable (VBNC) state in water.
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PMID:Survival of enterohemorrhagic Escherichia coli O157:H7 in water. 970 45

The ability of estrogen to prevent glucocorticoid-induced apoptosis in osteoblasts was studied both in vitro and in vivo. Glucocorticoid treatment for 72 h produced a dose-dependent increase in the number of apoptotic cells, determined by acridine orange/ethidium bromide staining, with a maximal response of 31+/-2% and 26+/-3% with 100 nM corticosterone in primary rat and mouse osteoblasts, respectively. Simultaneous administration of varying concentrations of 17beta-estradiol and 100 nM corticosterone decreased apoptotic osteoblasts in a dose-dependent manner, with a maximal decrease of 70% with 0.01 nM 17beta-estradiol. Terminal deoxynucleotidyltransferase-mediated deoxy-UTP-biotin nick end labeling also demonstrated glucocorticoid-induced DNA fragmentation that was inhibited by estrogen. Estrogen was shown to inhibit apoptosis induced by lipopolysaccharide treatment. As early as 6 h, Western blots demonstrated a dose-dependent decrease in the Bcl-2/Bax ratio, which reached a minimum of 0.18 in osteoblasts treated with 1000 nM corticosterone for 72 h. This reduction in Bcl-2/Bax was abolished by treating osteoblasts simultaneously with 17beta-estradiol, but not with 17alpha-estradiol. In 7-day-old mice, administration of varying concentrations of dexamethasone for 72 h resulted in a dose-dependent increase in the number of apoptotic osteoblasts as demonstrated by in situ terminal deoxynucleotidyltransferase-mediated deoxy-UTP-biotin nick end labeling staining of calvaria. A maximum of 22+/-1% apoptotic osteoblasts on the bone surface was found with 1 mg/kg BW dexamethasone compared with 2+/-1% in vehicle-treated mice. Injection of varying concentrations of 17beta-estradiol (0.5-5 mg/kg BW), but not 17alpha-estradiol, with 1 mg/kg dexamethasone produced a dose-dependent decrease in the number of apoptotic osteoblasts to 5+/-1% with 5 mg/kg 17beta-estradiol. Thus, glucocorticoid-induced apoptosis of osteoblasts may be prevented at least in part by 17beta-estradiol.
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PMID:Estrogen prevents glucocorticoid-induced apoptosis in osteoblasts in vivo and in vitro. 1053 65

Platelets and leukocytes are thought to play a leading role in the pathogenesis of many inflammatory conditions. To recruit flowing blood cells to the inflammatory region, it would be necessary for them to interact with vascular endothelial cells. Recently, many reports have indicated the resistance of spontaneous hypertensive rats (SHR) to endotoxic sepsis. Their resistance might be derived from suppressed interaction between these blood cells and endothelial cells. Therefore, SHR and age-matched Wistar-Kyoto rats (WKY) were induced with endotoxic sepsis by intravenous injection of lipopolysaccharide (LPS). At 4, 12, 24, and 48 hours after induction, leukocyte-endothelial interactions in the retina were evaluated in vivo with acridine orange digital fluorography. Fluorescently labeled platelets were also injected to investigate platelet-endothelial interactions in the retina in endotoxic sepsis. Leukocyte rolling in SHR after LPS injection was significantly suppressed; the maximum number of rolling leukocytes was reduced by 80.1% at 12 hours after LPS injection in SHR compared with WKY. Subsequent leukocyte infiltration into the vitreous cavity was significantly inhibited in SHR. Furthermore, platelet-endothelial interactions in the retina were also suppressed in SHR treated with LPS. The maximum numbers of rolling and adherent platelets were reduced by 59.5% and 62.6%, respectively, in SHR compared with WKY. In both strains, leukocyte- and platelet-endothelial interactions were substantially inhibited by the blocking of P-selectin. These suppressed interactions could contribute to the reduction of leukocyte- and platelet-mediated tissue injury in endotoxic sepsis in SHR, resulting in their resistance to endotoxemia.
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PMID:Interactions between blood cells and retinal endothelium in endotoxic sepsis. 1094 86

Previous studies have indicated that splenic macrophages migrate into the liver and play a role in endotoxin-induced hepatic damage. The present study was designed to elucidate the mechanisms of hepatocyte injury induced by activated splenic macrophages, focusing especially on endogenously released NO and oxidative DNA alterations in hepatocytes. Splenic macrophages isolated from Wistar rats were incubated with either lipopolysaccharide (LPS) or interferon-gamma (IFN-gamma) and cocultured with hepatocytes. Nitrite and nitrate levels in the culture medium were measured, and inducible-type NO synthase (iNOS) and nitrotyrosine were determined by immunofluorescence staining. The ratio of 8-hydroxy-deoxyguanosine (8-OH-dG) to deoxyguanosine (dG) was measured by high-performance liquid chromatography, and single-stranded DNA in hepatocytes was detected with acridine orange. NO release and nitrotyrosine expression in hepatocytes increased after 8 h of coculture with activated macrophages, and this coculture also induced increases in the 8-OH-dG/dG ratio and single-stranded DNA in the hepatocytes. These alterations were attenuated by superoxide dismutase (SOD) and NO synthesis inhibitors. A similar pattern of alterations was observed in hepatocytes incubated with SIN-1, and these changes were also prevented by SOD. These results suggest that activated macrophage-derived NO and its oxidative metabolite, peroxynitrite, play key roles in hepatocyte injury during inflammation, and cause subsequent DNA damage in surviving hepatocytes.
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PMID:Hepatocellular oxidative DNA injury induced by macrophage-derived nitric oxide. 1131 82


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