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

The Helicobacter pylori infections are followed by an infiltration of the gastric mucosa by neutrophils and macrophages. Accumulation of phagocytes enables them to interact with H. pylori, but a great number of infected subjects cannot eradicate these bacteria. The H. pylori inhibits its own uptake by blocking the function of phagocytes. The anti-phagocytic mechanism depends on bacterial surface structures and the presence of the cag pathogenicity island (PAI). The role of H. pylori lipopolysaccharide (LPS), during phagocytosis of these bacteria is not clear. LPS may mediate direct bacteria/phagocyte interactions and it may also regulate antibacterial activity of the phagocytes. In this study we investigated the influence of H. pylori LPS on phagocytosis of these bacteria. The H. pylori LPS inhibited an ingestion of these microbes by human peripheral blood granulocytes. This was correlated with a diminished ability of phagocytes to reduce MTT-tetrazolium salt. The anti-phagocytic effect of H. pylori LPS was reduced by recombinant lipopolysaccharide binding protein (rLBP). It is possible that in vivo H. pylori LPS may diminish elimination of these bacteria from the gastric mucosa promoting an infection persistence. However, LBP may modulate the uptake of H. pylori due to neutralization of anti-phagocytic effect of its LPS.
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PMID:Anti-phagocytic activity of Helicobacter pylori lipopolysaccharide (LPS)--possible modulation of the innate immune response to these bacteria. 1900 38

The study investigated the effects of red clover extract (RCE) on mouse T macrophages and lymphocytes in vitro. The cell toxic effect of RCE was estimated by MTT assay. Multiple-fluorescence staining plus flow cytometry were used to detect the effect of RCE on CD69/CD25/CD71 expression of mouse T lymphocytes stimulated by Con A; CFDA-SE staining plus flow cytometry were used to analyze the effect of RCE on proliferation of T lymphocytes activated by Con A; The effect of RCE on nitric oxide (NO) secretion of mouse macrophages stimulated by lipopolysaccharide (LPS) for 24 h was assayed by Griess reagent system. We found that RCE had potent anti-inflammatory effects on mice. RCE had little cell toxic effect on mouse lymphocytes and macrophages. RCE strongly inhibited the excessive production of inflammatory mediators (NO, CD69, CD25, CD71), in a dose-dependent manner, like cyclosporine A injection. RCE could inhibit proliferation of CD3+ T lymphocytes. These data suggested that RCE might exhibit anti-inflammatory effect by inhibiting the activation and proliferation of mouse lymphocytes and the NO secretion of mouse macrophages.
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PMID:Effects of red clover extract on the activation and proliferation of mouse T lymphocytes and the NO secretion of mouse macrophages. 1912 65

Inflammation is a major contributing factor to many blinding disorders including uveitis, diabetic retinopathy, and age-related macular degeneration. Here we examined the response of the retinal pigment epithelium (RPE) to physiological levels of lipopolysaccharide (LPS) to understand the role of this epithelium in inflammatory retinal conditions. Expression of a group of inflammatory mediators was identified by gene array analysis and confirmed by PCR and immunocytochemistry in primary human RPE cultures and ARPE19. The effects of LPS on the expression of these cytokines and RPE survival were examined by PCR, Luminex bead, and MTT assays. RPE cells express many cytokine receptors including IL-1R, -4R, -6R, -8RA, IFNAR1, IFNGR1/2 and secrete a range of pro- and anti-inflammatory cytokines including IL-4, -6, -8, -10, -17, IFN-gamma, MCP-1, and VEGF. LPS increases IL-13RA1 and IFNAR1, and decreases IL-7R receptor expression. It also increases RPE secretion of IL-4, -6, -8, -10, IFN-gamma and MCP-1, and is toxic to RPE cells at LC(50)=17.7 microg/ml. LPS toxicity is mediated by IL-6 and IL-8 through an autocrine feedback loop. Silencing IL-6R and IL-8RA gene expression by siRNA blocks death by their respective ligands or LPS. These findings imply that RPE cells are acutely sensitive to inflammatory stress and that over secretion of IL-6 and IL-8 by this epithelium during inflammatory stimulus may be an underlying factor in the progression of some retinal pathologies.
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PMID:Bacterial endotoxin activates retinal pigment epithelial cells and induces their degeneration through IL-6 and IL-8 autocrine signaling. 1915 52

Aqueous dispersible detonation nanodiamonds (NDs) with a diameter of 2-8 nm were assembled into a closely packed ND multilayer nanofilm with positively charged poly-L-lysine via the layer-by-layer deposition technique. The innate biocompatibility of the NDs in both free-floating and thin-film forms was confirmed via cellular gene expression examination by real-time polymerase chain reaction as well as MTT and DNA fragmentation assays. The highly biologically amenable ND nanofilm was successfully integrated with therapeutic molecules, and the functionality of the composite drug-ND material was assessed via interrogation of the suppression of inflammatory cytokine release. Knockdown of lipopolysaccharide-mediated inflammation was observed through the potent attenuation of tumor necrosis factor-alpha, interleukin-6, and inducible nitric oxide synthase levels following ND nanofilm interfacing with RAW 264.7 murine macrophages. Furthermore, basal cytokine secretion levels were assessed to examine innate material biocompability, revealing unchanged cellular inflammatory responses which strongly supported the relevance of the NDs as effective treatment platforms for nanoscale medicine. In addition to the easy preparation, robustness, and fine controllability of the film structures, these hybrid materials possess enormous potential for biomedical applications such as localized drug delivery and anti-inflammatory implant coatings and devices, as demonstrated in vitro in this work.
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PMID:Protein-mediated assembly of nanodiamond hydrogels into a biocompatible and biofunctional multilayer nanofilm. 1920 20

Recent studies brought evidence regarding the potential beneficial effects of cranberry polyphenols for periodontal infections. In this study, we evaluated the capacity of a proanthocyanidin-rich cranberry fraction to protect macrophages and oral epithelial cells against cytotoxicity induced by bacterial components. U937 cells, differentiated into adherent macrophage-like cells, as well as oral epithelial cells were treated with cell wall or lipopolysaccharide preparations from periodontopathogens. Cell viability was monitored using a commercial MTT (3-[4,5-diethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay. The cytoprotective effect was evaluated by pre-incubating human cells with a proanthocyanidin-rich cranberry fraction prior to treatment with the bacterial components at toxic concentrations. Among the various bacterial components tested, Peptostreptotoccus micros cell wall was found to be the most toxic for macrophages and epithelial cells and was thus selected for further analyses. Treatment of monocyte-derived macrophages with cell wall of P. micros (20 microg/ml) decreased the cell viability by approximately 50%. Adding the cranberry fraction prior to treating cells with P. micros cell wall dose-dependently protected monocyte-derived macrophages from the toxic effect. A dose-dependent cytoprotective effect of the cranberry fraction was also observed with oral epithelial cells treated with P. micros cell wall. This study suggests that cranberry polyphenols may exert a protective effect for host cells against the toxicity induced by bacterial components.
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PMID:Cytoprotective effect of proanthocyanidin-rich cranberry fraction against bacterial cell wall-mediated toxicity in macrophages and epithelial cells. 1927 73

Macrophages are critical cells in mediating the pathology of neurodegenerative disorders and enhancement of neuronal outward potassium (K(+)) current has implicated in neuronal apoptosis. To understand how activated macrophages induce neuronal dysfunction and injury, we studied the effects of lipopolysaccharide (LPS)-stimulated human monocytes-derived macrophage (MDM) on neuronal outward delayed rectifier K(+) current (I(K)) and resultant change on neuronal viability in primary rat hippocampal neuronal culture. Bath application of LPS-stimulated MDM-conditioned media (MCM) enhanced neuronal I(K) in a concentration-dependent manner, whereas non-stimulated MCM failed to alter neuronal I(K). The enhancement of neuronal I(K) was repeated in a macrophage-neuronal co-culture system. The link of stimulated MCM (MCM(+))-associated enhancement of I(K) to MCM(+)-induced neuronal injury, as detected by PI/DAPI (propidium iodide/4',6-diamidino-2-phenylindol) staining and MTT assay, was demonstrated by experimental results showing that addition of I(K) blocker tetraethylammonium to the culture protected hippocampal neurons from MCM(+)-associated challenge. Further investigation revealed elevated levels of K(v) 1.3 and K(v) 1.5 channel expression in hippocampal neurons after addition of MCM(+) to the culture. These results suggest that during brain inflammation macrophages, through their capacity of releasing bioactive molecules, induce neuronal injury by enhancing neuronal I(K) and that modulation of K(v) channels is a new approach to neuroprotection.
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PMID:Enhancement of neuronal outward delayed rectifier K+ current by human monocyte-derived macrophages. 1930 67

Dental endodontic sealers are in intimate contact with tissues around the root apex (periapical area) for extended periods. New endodontic sealers have been developed in the past decade, but the biological responses to many new products are not well documented. In this study, we assessed in vitro monocytic cytotoxic and inflammatory responses to several contemporary endodontic sealers. AH-Plus (AH), Pulp Canal Sealer (PC), Epiphany (EPH), Endo-Rez (ER), and an experimental Endo-Rez (ERx) were initially placed in buffered-saline for 12 weeks to simulate in vivo use. After "aging," specimens were placed in direct contact with THP1 monocytes for 72 h and their cytotoxicity (mitochondrial response; MTT) or ability to trigger or suppress cytokine secretion (ELISA; TNFalpha, IL1beta, IL=6; +/- lipopolysaccharide (LPS) exposure) were measured relative to Teflon (Tf) negative controls. Cellular responses among conditions were compared with ANOVA and Tukey post-hoc analysis (alpha = 0.05). Two of the five sealers, EPH and PC, still suppressed cell mitochondrial activity by 70% or more after 12 weeks of conditioning in saline. No sealer alone activated monocytic TNFalpha, IL1beta, or IL6 secretion (p > 0.05 vs. +LPS controls). When THP1 were activated by LPS after exposure to the sealers, differential suppression of TNFalpha, IL1beta, and IL6 secretion was observed for two of the five sealers tested. (EPH and PC) This data suggest that common endodontic sealers do not activate monocytic TNFalpha, IL1beta, and IL6 secretion in vitro by themselves, but degradation products of the sealers may suppress activation of monocytes.
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PMID:Inflammatory suppression by endodontic sealers after aging 12 weeks In vitro. 1957 99

The present work was carried out to elucidate the role of NSAIDs, PPARg agonist and HMG CoA inhibitor on cholesterol and lipopolysaccharide (LPS) induced neurodegeneration. The cerebellar, neuronal cells were exposed to cholesterol (10 and 50 microg/ml), LPS (1 ng/ml) or both. Neuroprotective effect of ibuprofen, rofecoxib, simvastatin and pioglitazone was assessed by measuring the neuronal loss, MTT dye assay, nitric oxide, LDH and lipid peroxide measurement. The results indicated that incubation of cholesterol and LPS showed less synaptic connections, neurite outgrowth and cell shrinkage as compared to normal cerebellar cells. Significantly decreased survival cells count along with increased LDH, lipid peroxide and nitrite levels were observed in the cells that confirmed neurodegeneration with cholesterol and LPS challenge. In comparison to individual toxins (LPS or cholesterol), combination of LPS and cholesterol produced more deleterious effect indicated synergistic effect of toxins. Interestingly, in comparison to LPS, cholesterol produced significantly low level of nitrites, LDH and lipid peroxides which indicated excessive cholesterol might not influence radical generation directly and might be a secondary effect. Among the drugs studied, NSAIDs showed better effect indicated inflammatory mediator response played vital role in cholesterol and LPS induced neurodegeneration. Simvastatin demonstrated moderate neuroprotective effect. It could be concluded that excessive cholesterol might produce cell death and led to release of nitrites and other cytokines. NSAIDs had better neuroprotective activity than simvastatin that produced moderate effect.
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PMID:Effect of excessive cholesterol and lipopolysaccharide on cerebellar neuronal cells in in vitro and protective role of anti-inflammatory drugs. 1957 95

Neural progenitor cells (NPC) are self-renewing multipotent cells that generate neurons and glial cells in the brain. NPCs generate neurons and glia not only during development but also after neural injury. Recent studies have shown that endogenous NPCs are activated after brain injury and migrate toward damaged areas where astrocyte activation occurs. Considering the massive proliferation of astrocytes as well as the production of several kinds of cytoactive molecules after brain injury, such as NO, growth factors and cytokines, it is tempting to think that cytoactive molecules released by activated glial cells regulate neural progenitor differentiation and proliferation through inflammatory mediators. To test this hypothesis, we stimulated rat primary astrocytes with lipopolysaccharide (LPS) to induce the activation of astrocytes. After addition of the conditioned media from LPS-stimulated astrocytes to NPC culture, proliferation was examined by MTT assay and bromodeoxyuridine (BrdU) incorporation. The differentiation of NPC into neurons and astrocytes was examined by Western blot, ELISA and immunocytochemical staining with cell-type-specific markers. Conditioned media from LPS-stimulated astrocytes increased NPC proliferation as well as gliogenesis as compared with control conditioned media from astrocytes without LPS stimulation. In contrast, neurogenesis was decreased by LPS-conditioned media. To investigate the molecular mechanism mediating glial differentiation and proliferation of NPC by reactive astrocytes, we added inhibitors of the Erk and JNK pathways during LPS stimulation. These inhibitors - except for a p38 inhibitor - decreased NPC proliferation and glial differentiation. These results suggest that LPS stimulated astrocytes generate factors regulating NPC proliferation and gliogenesis via the Erk and JNK pathways.
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PMID:Increased proliferation and gliogenesis of cultured rat neural progenitor cells by lipopolysaccharide-stimulated astrocytes. 1960 85

Granulocyte-colony stimulating factor (G-CSF) has recently been noted for neuroprotective function. Evidence has been given to indicate that G-CSF is naturally expressed in neurons and directly activates anti-apoptosis pathways. Finding out the agents inducing G-CSF production is of value for understanding the neuroprotection network in central nervous system. It is known that lipopolysaccharide (LPS) can induce macrophages to produce G-CSF. Here we demonstrate that hippocampal neurons exhibited the expression of toll-like receptor-4, and prove that low-dose LPS treatment increased the expression and production of G-CSF mRNA and protein in cultured neurons. We further indicate that the neutralization of G-CSF with corresponding anti-G-CSF antibodies abolished the neuroprotective effect of LPS pretreatment in N-methyl-D-aspartic acid-induced neuronal injury by MTT/CCK-8 assays and LDH release. Thus our results reveal that G-CSF may be involved in LPS-mediated neuroprotection in vivo.
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PMID:Granulocyte-colony stimulating factor is involved in low-dose LPS-induced neuroprotection. 1973 8


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