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Query: UNIPROT:P43026 (
lipopolysaccharide
)
62,215
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Brucella endotoxin differs from other gramnegative endotoxins in that it is recovered in the phenol phase rather than the aqueous phase of the Westphal hot phenol water procedure. This was the first described from this laboratory by Redfearn (1960) with phenol-killed smooth B. abortus and B. melitensis and has since been confirmed by others. Preliminary extraction of brucella cells with acetone, as called for in the original Westphal procedure, was followed by Renoux et al. (1973) who reported that the aqueous phase lacked endotoxic activity and the phenol phase had very low toxicity. In order to test the hypothesis that prior acetone extraction removes lipid A, we have repeated the Redfearn procedure with acetone extracted cells and have confirmed that the major portion of the endotoxic activity resides in the phenol phase. Acetone treatment does not remove the lipid A believed to be responsible for mouse lethality as well as necrotizing activity in guinea pig and rabbit skin. Preparations of brucella endotoxin (
lipopolysaccharide
) contain varying amounts of
polypeptide
some of which is tightly bound. The dermal response of sensitized guinea pigs to brucella LPS was shown to be a combination of reactions comprising those due to (1) innate toxicity of lipid A, (2) antibody mediated reactions due to polysaccharide portion of the molecule and (3) delayed hypersensitivity due to
polypeptide
portion of the molecule.
...
PMID:Studies of Brucella lipopolysaccharide. 126 51
In this article, we report on the nucleotide sequences of the rol genes of Escherichia coli O75 and Salmonella typhimurium LT2. The rol gene in E. coli was previously shown to encode a 36-kDa protein that regulates size distribution of the O-antigen moiety of
lipopolysaccharide
. The E. coli and S. typhimurium rol gene sequences consist of 978 and 984 nucleotides, respectively. The homology between the nucleotide sequences of these two genes was found to be 68.9%. Both the E. coli rol and S. typhimurium rol genes are transcribed counter to the histidine operon and code for deduced polypeptides of 325 and 327 amino acids, respectively. The S. typhimurium rol gene was previously identified to encode a protein of unknown function and to share a transcription termination region with his. The homology between these deduced
polypeptide
sequences was observed to be 72%. A complementation test was performed in which the S. typhimurium rol gene was placed in trans with an E. coli plasmid (pRAB3) which encodes the O75 rfb gene cluster and not rol. The protein expressed from the S. typhimurium rol gene was found to regulate the distribution of the O75 O polysaccharide on the
lipopolysaccharide
of the host strain, E. coli S phi 874. The mechanism of Rol action may be independent of O antigen subunit structure, and its presence may be conserved in members of the family Enterobacteriaceae and other gram-negative bacilli that express O polysaccharides on their surface membrane.
...
PMID:Nucleotide sequences of the genes regulating O-polysaccharide antigen chain length (rol) from Escherichia coli and Salmonella typhimurium: protein homology and functional complementation. 137 82
Cyclooxygenase (Cox), also known as prostaglandin (PG) H synthase (EC 1.14.99.1), catalyzes the rate-limiting step in the formation of inflammatory PGs. A major regulatory step in PG biosynthesis is at the level of Cox: growth factors, cytokines, and tumor promoters induce Cox activity. We have cloned the second form of the Cox gene (Cox-2) from human umbilical vein endothelial cells (HUVEC). The cDNA encodes a
polypeptide
of 604 amino acids that is 61% identical to the previously isolated human Cox-1
polypeptide
. In vitro translation of the human (h)Cox-2 transcript in rabbit reticulocyte lysates resulted in the synthesis of a 70-kDa protein that is immunoprecipitated by antiserum to ovine Cox. Expression of the hCox-2 open reading frame in Cos-7 monkey kidney cells results in the elaboration of cyclooxygenase activity. hCox-2 cDNA hybridizes to a 4.5-kilobase mRNA species in HUVEC, whereas the hCox-1 cDNA hybridizes to 3- and 5.3-kilobase species. Both Cox-1 and Cox-2 mRNAs are expressed in HUVEC, vascular smooth muscle cells, monocytes, and fibroblasts. Cox-2 mRNA was preferentially induced by phorbol 12-myristate 13-acetate and
lipopolysaccharide
in human endothelial cells and monocytes. Together, these data demonstrate that the Cox enzyme is encoded by at least two genes that are expressed and differentially regulated in a variety of cell types. High-level induction of the hCox-2 transcript in mesenchymal-derived inflammatory cells suggests a role in inflammatory conditions.
...
PMID:Human cyclooxygenase-2 cDNA. 138 Jan 56
Two monoclonal antibodies against Actinobacillus pleuropneumoniae serotype 5, designated as 5MAb-1 and 5MAb-6, were characterized. Enzyme-linked immunosorbent assay-inhibition tests with whole-cell antigens obtained from strains of serotype 1 through 12 of A pleuropneumoniae revealed that 5 MAb-1 bound to only serotype-5 strains. The epitope recognized by 5MAb-1 was a carbohydrate that was sensitive to periodate oxidation and resided on the structure of beta-1,6-linked D-galactose in an O-antigen polysaccharide of serotype-5
lipopolysaccharide
. Analysis of these results revealed that the O-antigen polysaccharide of
lipopolysaccharide
was 1 of the antigenic determinants responsible for the serotype specificity of A pleuropneumoniae. On the other hand, 5MAb-6 reacted with strains of serotype 1 through 10 in varying degrees and its epitope was located on polypeptides sensitive to proteinase K. In an immunoblotting analysis, 5MAb-6 reacted with 2
polypeptide
bands, with molecular weights of approximately 41,500 and 28,000, in the outer membrane protein-rich fraction obtained from strains of serotype 1 through 10. These results indicated that outer membrane proteins from several serotype strains of A pleuropneumoniae possessed common antigenic determinants.
...
PMID:Characterization of monoclonal antibodies against Actinobacillus pleuropneumoniae serotype 5. 138 4
Endothelial cell activation antigens may play important roles in immune responses and in inflammation. This report describes the identification and characterization of a monoclonal antibody, named EAA-B, which reacts specifically with human umbilical vein endothelial (HUVE) cells pre-treated with tumour necrosis factor-alpha (TNF-alpha) but not with untreated cells. The expression of the EAA-B antigen on HUVE cells could also be induced by interleukin-1 (IL-1), bacterial
lipopolysaccharide
(
LPS
), and phorbol esters but not by interferon-gamma (IFN-gamma). By contrast, EAA-B antigen expression on neonatal foreskin and rheumatoid synovial fibroblasts, whether pre-treated with TNF-alpha or not, was not detectable. Peripheral blood leucocytes and the leukaemic cell lines U937, HL-60, Raji and Molt 4 showed no detectable expression of the EAA-B antigen. Kinetic studies demonstrated that the EAA-B antigen was rapidly expressed, peaked at 6 hr and declined to basal level by 24 hr. Western blotting revealed that monoclonal antibody EAA-B recognized a
polypeptide
of approximately 80,000-90,000 MW. EAA-B partially blocked the augmented adhesion of HL-60 cells to TNF-treated HUVE cells. However, it failed to inhibit the enhanced binding of peripheral blood leucocytes, U937, Raji and Molt 4 Cells to TNF-treated HUVE cells. In situ, the EAA-B antigen was detected on some vascular endothelium in tonsils, lymph nodes, psoriatic skin and rheumatoid synovium but not in normal non-lymphoid tissues. Interestingly EAA-B antigen is also expressed by B lymphocytes in germinal follicle centres (GFC) of lymphoid tissues. The co-expression of this endothelial activation antigen by GFC B lymphocytes may have significant implications for immune responses and in B-lymphocyte differentiation.
...
PMID:Identification of a human endothelial cell activation antigen that is co-expressed by germinal follicle centre B lymphocytes. 139 50
Activin A/erythroid differentiation factor (EDF), a dimeric
polypeptide
hormone composed of two beta A subunits, regulates growth and erythroid differentiation of human hematopoietic progenitor and erythroleukemia cells. We have identified activated human peripheral blood monocytes as a natural source of activin A/EDF. In these cells,
lipopolysaccharide
(
LPS
) induced rapidly the expression of the beta A subunit mRNAs through protein kinase C-dependent transcriptional regulation. The beta A subunit mRNA expression was also increased by 1,25-dihydroxyvitamin D3, an inducer of macrophage maturation of monocytes. Western analysis with an anti-beta A antibody and an erythroid differentiation bioassay confirmed that the conditioned media of
LPS
-activated monocytes contained the activin A/EDF protein. We suggest that monocyte/macrophage-derived activin A/EDF may not only modulate hematopoiesis but may also act as a mediator molecule in the diverse physiologic and pathogenetic events in which these cells are involved.
...
PMID:Activin A/erythroid differentiation factor is induced during human monocyte activation. 140 87
The role that inflammatory cytokines may play in the life cycle of the hepatitis B virus and in the pathogenesis of its associated liver disease has not been carefully delineated. In this report, we demonstrate that bacterial
lipopolysaccharide
, a potent inducer of inflammatory cytokines in vivo, causes a severe acute liver disease in transgenic mice whose hepatocytes produce the hepatitis B virus large envelope
polypeptide
and retain HBsAg within the endoplasmic reticulum. In contrast, 100-fold higher doses of bacterial
lipopolysaccharide
do not induce liver cell injury in nontransgenic littermate controls or in transgenic mice whose hepatocytes secrete HBsAg rather than retain it. Coincident with the hepatocellular injury and the influx of inflammatory cells into the liver, a marked reduction occurs in the intrahepatic content of hepatitis B virus steady-state messenger RNA, thereby confirming the selectivity of this process for the HBsAg-positive hepatocyte. Bacterial
lipopolysaccharide
-induced hepatocellular injury appears to be principally mediated by interferon-gamma because it can be markedly reduced by the prior administration of neutralizing interferon-gamma-specific monoclonal antibodies and because recombinant interferon-gamma is also selectively cytotoxic for the HBsAg-positive transgenic hepatocyte in vivo. Tumor necrosis factor-alpha is also involved in this process because bacterial
lipopolysaccharide
-induced liver cell injury is significantly reduced by tumor necrosis factor-alpha specific monoclonal antibodies. The role of tumor necrosis factor-alpha in bacterial
lipopolysaccharide
-induced liver cell injury is less clear than interferon-gamma, however, because unlike interferon-gamma it is also toxic for nontransgenic hepatocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:HBsAg retention sensitizes the hepatocyte to injury by physiological concentrations of interferon-gamma. 150 8
Interleukin 1 receptor antagonist (IL-1ra), a naturally occurring
polypeptide
with amino acid sequence homology to interleukin 1 alpha (IL-1 alpha) and interleukin 1 beta (IL-1 beta), prevents Escherichia coli-induced shock and death. Both IL-1 and IL-1ra are produced by monocytes stimulated with
lipopolysaccharide
(
LPS
). Because interleukin 4 (IL-4) suppresses IL-1 production, we investigated whether IL-4 modulated IL-1ra synthesis in
LPS
-stimulated human peripheral blood mononuclear cells. IL-1 beta and IL-1ra were measured by specific RIAs. IL-4 alone (0.01-100 ng/ml) did not stimulate IL-1 beta synthesis but rather induced IL-1ra (4.82 +/- 0.94 ng/ml).
LPS
induced synthesis of both IL-1 beta (6.67 +/- 1.06 ng/ml) and IL-1ra (10.77 +/- 2.79 ng/ml). IL-4 suppressed
LPS
-induced IL-1 beta mRNA accumulation and synthesis. However, IL-4 acted synergistically with
LPS
in inducing IL-1ra. IL-4 enhanced
LPS
-induced IL-1ra mRNA accumulation 4-fold and IL-1ra protein synthesis nearly 2-fold. Moreover, IL-1ra mRNA levels were maximal after 6 hr of exposure to
LPS
but peaked within the first 3 hr in the presence of IL-4. IL-4 added as late as 12 hr after
LPS
stimulation still enhanced IL-1ra synthesis. In human peripheral blood mononuclear cells stimulated with IL-1 alpha, IL-4 markedly suppressed IL-1 beta production but enhanced IL-1ra synthesis greater than 2-fold. Because IL-4 favors synthesis of the natural antagonist IL-1ra over synthesis of the agonist IL-1, IL-4 may exert potent antiinflammatory effects on host responses to Gram-negative infections.
...
PMID:Coordinated antiinflammatory effects of interleukin 4: interleukin 4 suppresses interleukin 1 production but up-regulates gene expression and synthesis of interleukin 1 receptor antagonist. 153 84
The aromatic-dependent live Shigella flexneri Y strain SFL114, attenuated by a Tn10-inactivated aroD gene, was given as an oral vaccine to 14 Macaca fascicularis monkeys. A significant clinical attenuation of SFL114 was seen (p = 0.0058) as all vaccinated monkeys tolerated 2 x 10(10)-1 x 10(11) bacteria of SFL114, whereas four out of seven monkeys orally given 1 x 10(11) of the virulent parent strain SFL1 developed shigellosis. The average excretion time for SFL114 and SFL1 were 2 and 18 days, respectively. As seen endoscopically SFL1 caused colonic lesions, whereas SFL114 did not. Histopathologic examination of colonic biopsies showed that SFL114 induced only slight acute inflammation, whereas SFL1 caused severe acute inflammation (p less than 0.01). The vaccine strain SFL114 elicited significant species-specific serum immune responses (p less than 0.005) as seen in enzyme immune assays using lipopolysaccharides from S. flexneri serotypes Y, 1b, and 2a and Escherichia coli K-12 as antigens. The titres were comparable to those seen in monkeys given virulent S. flexneri strains. Western blot analyses showed that many prevaccination sera contained antibodies directed against the invasion plasmid-coded polypeptides. However, after vaccination with SFL114 increased amounts of such anti-
polypeptide
antibodies were seen, particularly in sera from monkeys having a low prevaccination antibody level. SFL114 also elicited a significant species-specific (p less than 0.025) local intestinal sIgA response against the homologous
lipopolysaccharide
antigen. Vaccinated monkeys were clinically protected against an oral challenge with 1-2 x 10(11) live, virulent S. flexneri strains of any of serotypes Y (strain SFL1), 1b (strain SFL27), or 2a (strain M4243).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Auxotrophic live oral Shigella flexneri vaccine protects monkeys against challenge with S. flexneri of different serotypes. 155 32
Two dimensional gel electrophoresis (2-D PAGE) and automated image analysis were used to study the effects of bacterial
lipopolysaccharide
(
LPS
) activation on secreted and cellular rat alveolar macrophage proteins. Primary alveolar macrophages were cultured and exposed to
LPS
in the presence of [35S]-methionine for 24 h. Image analysis of 2-D PAGE revealed that
LPS
treatment primarily modulated the proportions of several alveolar macrophage cellular proteins versus control in addition to limited protein induction and repression. The differential effect of
LPS
was more pronounced on secreted proteins where qualitative and quantitative differences from control cells were found. Immunoblots of secreted proteins with anti-tumor necrosis factor alpha (TNF alpha) and anti-interleukin-1 alpha(IL-1 alpha) antibodies identified these monokines from protein fluorographic patterns. IL-1 alpha was detected as a single
polypeptide
of 17 kD at pI = 5. Use of recombinant TNF alpha and monoclonal and polyclonal antibodies for immunodetection revealed the 17 kD form of TNF alpha as well as higher molecular weight species at 18 kD and 22 kD. Thus, analysis of radiolabeled rat macrophages treated with
LPS
reveals quantitative modulation of several cellular proteins as well as a distinctive pattern of secreted proteins which contain multiple monokine forms resolvable by 2-D PAGE.
...
PMID:Two dimensional gel electrophoresis of cellular and secreted proteins from rat alveolar macrophages after lipopolysaccharide treatment. 156 19
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