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)

To identify the mediators that stimulate periapical bone resorption following infection, a rat model system was used in which active (rapid) and chronic (slow) phases of bone destruction can be distinguished. Extracts of inflammatory tissues from active lesions contained high levels of bone-resorbing activity, which was destroyed by proteinase K and heat (70 degrees C), but was unaffected by polymyxin B, indicating the presence of protein mediator(s) rather than lipopolysaccharide. Fast-performance liquid chromatography gel filtration of extracts of active lesions demonstrated that most activity was associated with macromolecules of MW 30-60 kDa and 15-20 kDa, consistent with bone resorptive cytokines, including interleukin 1 (IL-1) and tumor necrosis factor (TNF). Inhibition with cytokine-specific antisera demonstrated that resorbing activity in active lesions was significantly neutralized by anti-IL-1 alpha, whereas anti-IL-1 beta, anti-TNF alpha and anti-TNF beta had only slight effect. A lower amount of resorbing activity was present in extracts of chronic lesions, which was also neutralized only by anti-IL-1 alpha. Inflammatory tissue explants produced more IL-1 alpha than IL-1 beta in vitro, confirming findings with extracts, and high levels of IL-1 alpha were present in active lesions by radioimmunoassay. These data indicate that bone resorption stimulated by bacterial infection is primarily mediated by IL-1 alpha in this model. The similarity of cytokines in active and chronic lesions suggests that quantitative rather than qualitative differences in these mediators may account for lesion progression.
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PMID:The role of interleukin-1 alpha in the pathogenesis of periapical bone destruction in a rat model system. 851 Sep 85

In the previous paper (Takeda et al, Int. Immunol., 5, 691-694, 1993), we demonstrated that tumor necrosis factor-alpha (TNF-alpha) promptly accelerates apoptosis of human neutrophils in vitro. In order to determine the role of neutrophil apoptosis in defending against bacterial infection, we studied the effect of bacterial lipopolysaccharide (LPS) on this process. LPS inhibited spontaneous and TNF-alpha-induced human neutrophil apoptosis in vitro, as determined by 1) light and electron microscopy, 2) flow cytometry, and 3) agarose gel electrophoresis of DNA. Low concentrations of cycloheximide, a protein synthesis inhibitor, which alone did not affect neutrophil apoptosis, were able to reduce spontaneous apoptosis inhibition by LPS, suggesting the involvement of newly synthesized protein in this phenomenon.
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PMID:Inhibition by bacterial lipopolysaccharide of spontaneous and TNF-alpha-induced human neutrophil apoptosis in vitro. 857 86

The cascade of physiologic mechanisms in response to infection, the acute phase response, is recognized as having a major role in host defense. Two such responses are an increase in plasma copper and activation of the hypothalamic-pituitary-adrenal axis, which are consistently reported to occur during bacterial infection. We aimed to determine whether the alterations in plasma copper and corticosterone were conditionable using the conditioned taste aversion paradigm. The regime involved the pairing of a novel-tasting saccharine solution (the conditioned stimulus) with lipopolysaccharide (the unconditioned stimulus). Seven days after the initial pairing of these stimuli (the test day), the saccharine solution was represented. Animals exposed to this condition displayed a significant decrease in plasma copper levels. In addition, these rats experienced a reduction in plasma corticosterone that was time dependent. Paradoxically, the conditioned response of both these variables were in a direction contrary to that reported during bacterial infection. These results suggest that some acute phase responses may condition as a rebound response, or in an opposing trend to that occurring as the initial reaction.
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PMID:Paradoxical conditioning of the plasma copper and corticosterone responses to bacterial endotoxin. 857 1

The effect of chronic ethanol ingestion on class-specific immunoglobulin (Ig) synthesis after burn injury was investigated in C57BL/6 mice. Animals were divided into four groups: control, burn, ethanol-sham, and ethanol-burn groups. Five days after injury or the last ethanol ingestion, cell suspensions from spleen and mesenteric lymph nodes were prepared. The number of class-specific Ig-bearing cells were counted by flow cytometry. The cell suspensions were cultured with lipopolysaccharide for 4 days. The supernatants from these cultures were tested for class-specific Ig by enzyme-linked immunoassay. No change occurred in the amount of class-specific IgG and IgA produced by 10(5) lymphocytes calculated from both of these data. Both burn and ethanol alone impaired IgM synthesis; splenic IgM was most affected by burn, and mesenteric lymph node IgM was most affected by ethanol. The group receiving ethanol before burn had IgM synthesis significantly impaired in both lymphocyte populations. Because IgM is the most important Ig in resistance to bacterial infection, this consistent suppression of IgM synthesis in both these tissues may contribute to increased incidence and severity of acute infection.
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PMID:Immunoglobulin M synthesis after burn injury: the effects of chronic ethanol on postinjury synthesis. 858 19

A genomic clone encoding a new member of attacin, an insect antibacterial protein, was isolated from a genomic library of the silkworm, Bombyx mori, and the nucleotide sequence of the 5'-upstream region was determined. The region contained Bm 1, a highly repetitive element of B. mori and a lipopolysaccharide (LPS) response element (RE)(NF-kappaB binding site), CAAT box and TATA box. Northern blot analysis showed that the attacin gene expression was rapidly induced by bacterial cell wall components such as LPS from Escherichia coli and peptidoglycan (PG) from Micrococcus luteus, suggesting that attacin plays an important role in an early phase of the self-defense system upon bacterial infection.
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PMID:Nucleotide sequence of 5'-upstream region and expression of a silkworm gene encoding a new member of the attacin family. 860 9

Bacterial infection stimulates the host to mount a rapid inflammatory response. A 6-base DNA motif consisting of an unmethylated CpG dinucleotide flanked by two 5' purines and two 3' pyrimidines was shown to contribute to this response by inducing polygonal B-cell activation. This stimulatory motif is 20 times more common in the DNA of bacteria than higher vertebrates. The current work shows that the same motif induces the rapid and coordinated secretion of interleukin (IL) 6, IL-12, and interferon gamma (but not IL-2, IL-3, IL-4, IL-5, or IL-10) in vivo and in vitro. Stimulatory CpG DNA motifs induced B, T, and natural killer cells to secrete cytokine more effectively than did lipopolysaccharide. Thus, immune recognition of bacterial DNA may contribute to the cytokine, as well as the antibody production characteristic of an innate inflammatory response.
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PMID:CpG motifs present in bacteria DNA rapidly induce lymphocytes to secrete interleukin 6, interleukin 12, and interferon gamma. 861 Jan 35

The murine S100 protein CP-10 is a potent chemotactic factor for murine and human myeloid cells in vivo and in vitro. This is the first report describing regulations of the CP-10 gene by a proinflammatory stimulus, lipopolysaccharide (LPS), in cells of the monocyte/macrophage lineage. Murine monocyte/macrophage-like WEHI 265 and RAW 264.7 cells preexposed to 5 to 50 ng/mL LPS expressed significant levels of CP-10 mRNA 4 hours, and maximal at 20 hours, after a secondary LPS challenge. This was accompanied by increasing levels of cell-associated and released CP-10 protein. In contrast, a single dose of LPS upregulated CP-10 mRNA in elicited peritoneal macrophages, whereas mRNA and protein levels decreased following LPS challenge. The state of macrophage differentiation may control responsiveness as LPS had no effect on CP-10 basal levels in bone marrow derived macrophages. LPS-induced CP-10 expression was controlled at the transcriptional level and nuclear run-on and protein synthesis inhibition assays indicated that LPS priming and challenge of RAW cells occurred via distinct pathways. MRP14, another S100 protein generally coordinately expressed with human MRP8, was not induced by LPS under the same conditions. We propose that CP-10 may play a key role in recruitment of leukocytes into tissues in response to gram-negative bacterial infection.
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PMID:Induction of the chemotactic S100 protein, CP-10, in monocyte/macrophages by lipopolysaccharide. 861 21

Fibronectin is a major product of fibroblasts and can mediate diverse functions including wound healing. Chronic bacterial infections are generally associated with a marked decreased in the ability to repair. We therefore hypothesized that bacterial endotoxin, lipopolysaccharide (LPS), might alter fibroblast fibronectin production. LPS augmented fibronectin production by fibroblasts and also stimulated the release of fibronectin from cell layers. An increase in new protein synthesis appeared to account for part of the increased fibronectin, because the inhibitor of protein synthesis, cycloheximide, inhibited the increase in total production of fibronectin. Cycloheximide did not attenuate the increased release of fibronectin into the culture medium. This increased release appeared to be caused, at least in part, by fragmentation of fibronectin by proteases contained in LPS preparations. In this regard all preparations of LPS tested were found to cleave fibronectin. Finally, zymograms indicated that LPS could also cleave gelatin with at least two bands of proteolytic activity but that it did not cleave bovine serum albumin or ovalbumin. These results indicate that the ability of bacterial products to alter fibronectin production and to degrade this macromolecule may account for altered wound repair that occurs with chronic bacterial infection.
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PMID:Lipopolysaccharide increases fibronectin production and release from cultured lung fibroblasts partially through proteolytic activity. 862 82

The etiology of chronic rejection is unknown, although acute rejection, viral infection, and initial graft ischemia have been implicated. To test the effects of infections on the process of chronic rejection, we simulated bacterial infection by the administration of the endotoxin lipopolysaccharide (LPS), a potent activator of various cell types in an established rat model of chronic rejection. Lewis recipients of Fisher 344 kidneys were treated with a single dose of LPS or vehicle 8 weeks following transplantation and grafts were examined at various time points. In the chronically rejecting controls, leukocytic infiltration and the expression of cytokines peaked at 16 weeks. In LPS-treated hosts, leukocyte infiltration and cytokine expression peaked at 12 weeks. By 16 weeks, glomeruli in LPS-treated recipients had become far more sclerotic than those in controls, mimicking the changes observed in controls at 24 weeks. We conclude that infections may play an important role in the development of chronic rejection.
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PMID:Infection-associated cellular activation accelerates chronic renal allograft rejection in rats. 863 55

Although burn wound excision and grafting have been shown to improve patient survival, the effects on immune function, especially humoral immunity, are not completely understood. The purpose of this study was to investigate the effect of immediate and early wound excision on antibody synthesis and B-cell proliferation, specifically, antibody response to PGPS, a ubiquitous bacterial cell wall antigen. Thirty-six male BALB/c mice were divided into four groups. Sham mice received no burn, and remaining mice received a 30% body surface area full-thickness burn. Under general anesthesia, excision and grafting was performed either 6 or 72 hr after injury (BE&G6 and BE&G72 groups). A fourth control group received burn but did not undergo excision and grafting (Burn group). Splenocytes were isolated 8 days postburn and stimulated with 2.5 microgram/ml lipopolysaccharide. Anti-PGPS IgM, total IgM, and total IgG levels were determined by ELISA. B-cell proliferation, measured by [3H]-thymidine uptake, was expressed as stimulation index. All B-cell functions were significantly suppressed by burn injury. Immediate excision and grafting (BE&G6) restored anti-PGPS IgM synthesis to normal, while nonspecific B-cell functions did not change significantly. Early excision and grafting (BE&G72), however, failed to significantly improve any B-cell functions. Immediate but not early BE&G restored antibody synthesis to the bacterial cell wall antigen (PGPS). Immediate BE&G may therefore lead to a decrease in bacterial infection after burn injury.
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PMID:Immediate burn wound excision restores antibody synthesis to bacterial antigen. 866 Nov 90


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