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)

A patient with Philadelphia chromosome (Ph1) positive chronic myelogenous leukemia (CML) entered a blast crisis localized to lymph nodes. On light microscopy, by morphology and histochemical staining, the blasts were undifferentiated. In spite of terminal deoxynucleotidyl transferase positivity, some of the lymph node cells expressed a myeloid differentiation antigen, OKM1, and were peroxidase positive by transmission electron microscopy (TEM). However, the majority of cells were peroxidase negative on TEM and expressed OKT-10, a marker found on both primitive myeloid and lymphoid cells. Cultures of lymph node cells stimulated with Epstein-Barr virus or lipopolysaccharide (LPS) revealed the Ph1, indicating B cell involvement in the CML. T cells from cultures stimulated with L4-phytohemagglutinin and T cell growth factor were negative for the Ph1. In unstimulated lymph node cells, the uncomplicated Ph1 could not be demonstrated; instead, a unique complex karyotype involving a masked Ph1 was identified in these and the LPS cultures. This karyotype was not found in bone marrow (BM) metaphase cells. Instead, BM cells showed either the simple Ph1 or the Ph1 with a rearrangement involving chromosomes 13 and 20. The patient had transient responses to three chemotherapy regimens, two of which were designed to treat acute lymphocytic leukemia, but he died 8 months after disease acceleration without BM blast crisis. These findings are compatible with an extramedullary blast crisis originating in a primitive cell with both myeloid and lymphoid characteristics.
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PMID:Unusual karyotypic changes and B cell involvement in a case of lymph node blast crisis of chronic myelogenous leukemia. 661 Apr 45

Using a sister chromatid differentiation technique, cell cycle study of stimulated lymphocytes of B-cell chronic lymphocytic leukemia (B-CLL) revealed their cell cycle progression to be similar to that of normal lymphocytes stimulated by T-cell and various polyclonal B-cell activators (PBA). The chromosome constitutions of stimulated lymphocytes in 62 patients with B-CLL were examined using PBA such as Epstein-Barr virus (EBV) and lipopolysaccharide W from E. coli 055:B5 (LPS). Of the 20 patients with abnormal clones, 11 patients had trisomy 12; other less common abnormalities were trisomy 1, 6q-, i(7q), 14q+, trisomy 16, trisomy 18, reciprocal translocations, and marker chromosomes of unknown origin. These findings indicate that trisomy 12 may be a unique and common karyotypic change in B-CLL. The fact that 3 out of 4 patients with marker chromosomes showed stage IV disease may indicate that a clone with a marker is a predictor of an unfavourable prognosis. The near correlation between trisomy 12 and kappa chains existed (0.05 less than p less than 0.10). Trisomy 12 was seen in all 5 patients with monoclonal paraprotein.
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PMID:Chromosome studies in stimulated lymphocytes of B-cell chronic lymphocytic leukemias. 661 Jun 24

Peripheral blood lymphocytes from 11 patients with chronic lymphocytic leukemia were stimulated by Epstein-Barr virus (EBV), lipopolysaccharide from Escherichia (LPS), and phytohemagglutinin (PHA). Chromosome analysis with the Q-banding technique after 5 days incubation revealed an extra chromosome 12 in 5 of the patients and a translocation between chromosome 11 and chromosome 14 in 1. Two patients had a deletion of chromosome 6, and only 3 patients had a normal karyotype. In most patients, the abnormalities were found in the majority of metaphases after stimulation with EBV, LPS, or both mitogens, while PHA revealed a normal karyotype, with the exception of a total of 4 metaphases in 3 patients. An extra chromosome 12 appears to be specifically associated with chronic lymphocytic leukemia. The frequency of chromosomal abnormalities in this disease appears to be much higher than has previously been thought.
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PMID:Nonrandom chromosomal aberrations in chronic lymphocytic leukemia revealed by polyclonal B-cell-mitogen stimulation. 696 31

Peripheral blood lymphocytes from 22 consecutive patients with chronic lymphocytic leukaemia were stimulated with the polyclonal B-cell mitogens lipopolysaccharide from E. coli (LPS) and Epstein-Barr virus (EBV). Stimulation was successful for chromosome analysis in 14 patients. Eleven patients had chromosomal aberrations and 7 of these had an extra chromosome 12. In 2 patients an extra chromosome 12 was the only abnormality, while additional aberrations were found in 5 patients. 3 patients had complex aberrations involving deletion of chromosome 6. 1 of these patients also had a translocation between chromosomes 12 and 14. 1 patient had a translocation between chromosomes 11 and 14. In 3 patients no aberrations were detected. The time elapsing between diagnosis and appearance of clinical symptoms which were indications for treatment was significantly shorter in patients with an extra chromosome 12 than in these without this abnormality. Thus, it appears that an extra chromosome 12 is associated with a more rapid course of the disease, and may therefore be of importance for the predition of prognosis.
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PMID:Extra chromosome 12 and prognosis in chronic lymphocytic leukaemia. 708 76

Human peripheral blood lymphocytes (PBL) were cultured for various time periods (up to 8 d) in the presence of pokeweed mitogen (PWM), lipopolysaccharide, or Epstein-Barr virus. Cell-free supernates were fractionated on a standardized ultrogel AcA 22 column and the proportion of polymeric and monomeric IgA was determined by radioimmunoassay. The results demonstrate that PBL stimulated with these mitogens produce IgM and IgG with molecular characteristics identical to those found in serum, but that the IgA produced is predominantly of the polymeric type. To prove that this IgA represented disulfide bond-linked polymers rather than aggregated monomers, we have demonstrated that the high molecular weight IgA (a) maintains its polymeric form upon treatment with acidic buffers, (b) contains J chain, a glycoprotein associated only with polymeric immunoglobulins, and (c) dissociates to the monomeric form upon reduction of disulfide bonds. After 1 wk in culture, approximately 60% of the PWM-stimulated cells that contained IgA were positive for IgA2, whereas 40% were IgA1 positive as determined by immunofluorescence. Therefore, peripheral blood contains a population of lymphocytes with the potential to display, after appropriate stimulation and differentiation, characteristics similar to IgA cells found in external secretory tissues. The demonstration of the presence of such cells in the peripheral circulation suggests that these cells are precursors of IgA-producing plasma cells with the potential to populate mucosal tissues.
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PMID:Production of predominantly polymeric IgA by human peripheral blood lymphocytes stimulated in vitro with mitogens. 743 Sep 51

Epstein-Barr virus (EBV) has a marked tropism for cells of the immune system, and infection can result in profound immunomodulatory effects. In order to examine the role of cytokines during the acute phase of infectious mononucleosis, we studied the levels of different interleukins (ILs), interferons (IFNs), and the soluble IL-2 receptor (sIL-2R) in serum samples of 20 patients. We found elevated levels of IL-2, IL-6, sIL-2R, and IFN-gamma. Whereas the peak of IL-2 and IL-6 concentration occurred during the first week (P < 0.01), the largest amounts of sIL-2R were measured during the second week (P < 0.01). IFN-gamma levels were only enhanced during the first week. In addition, we investigated the ability to produce cytokines in response to mitogenic stimulation in a whole-blood assay of 11 patients compared with healthy blood donors. In the whole-blood assay of patients compared with controls after stimulation with lipopolysaccharide, we measured more than 10-fold elevated levels of tumor necrosis factor alpha (P < 0.01), 3-fold elevated levels of IL-1 beta (P < 0.01), and about 2-fold increased amounts of IL-6 (P < 0.01). A significant enhancement in sIL-2R and IFN-gamma concentration was found in the assay after stimulation with phytohemagglutinin after 24 h of incubation (P < 0.01). Collectively, our data seem to indicate that monocytes are strongly activated during infectious mononucleosis. Monocytes and monocyte-derived factors may play an important role in the pathogenesis of infectious mononucleosis and, together with T lymphocytes, may be partly responsible for clinical symptoms.
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PMID:Cytokine production in a whole-blood assay after Epstein-Barr virus infection in vivo. 769 31

Clones encoding porcine interleukin 10 (IL-10) were isolated from a cDNA library produced from phytohemagglutinin-activated pig peripheral blood mononuclear cells. The porcine IL-10 nucleotide sequence was found to be highly homologous to the rat, mouse, and human IL-10 counterparts and to one of the open reading frames from the Epstein-Barr virus. In addition, pig IL-10 caused inhibition of gamma-interferon gene transcription as determined by a bioassay. To investigate the possible immunomodulatory role of IL-10, its expression during the induction of tolerance to kidney allografts by cyclosporin A in miniature swine was also investigated. Delayed expression and higher levels of IL-10 were observed in tolerant animals compared with animals rejecting their allografts. Since tolerance is achieved by a short course of cyclosporin A, we have also studied the in vitro effect of this drug on IL-10 gene transcription in blood mononuclear cells and have found that cyclosporin A inhibits IL-10 gene activation in T cells but does not interfere with IL-10 transcription in lipopolysaccharide-activated cells. These results suggest that the overexpression of IL-10, observed in cell populations infiltrating grafts from tolerant animals, may be a function of monocytes and/or B cells.
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PMID:Molecular identification of porcine interleukin 10: regulation of expression in a kidney allograft model. 770 27

The haemolytic uraemic syndrome, first described in 1955 by Gasser, is the number one cause of acute renal failure in infants. There are three types of the haemolytic uraemic syndrome: the seasonal epidemic form with prodromic diarrhoea and generally favourable outcome which usually occurs in infants, a less typical form without signs of digestive tract involvement and no seasonal prevalence which occurs more readily in older children and sometimes in families has a less favourable prognosis, and finally drug- or disease-related forms. Currently, overall mortality due to haemolytic uraemic syndrome has been reduced to about 4%, usually as a result of damage to the central nervous system. Several microorganism, including Shigella dysenteriae, Salmonella typhi, Campylobacter jejuni, Streptococcus pneumoniae, Rickittsiae and certain viruses (Coksackiae, Influenzae, Epstein-Barr) have been identified as causative agents. In 1983, digestive tract infection due to an Escherichia coli strain producing verotoxin was identified as capable of producing haemolytic uraemic syndrome and more rarely thrombopenic thrombotic purpura. The germ produces two exotoxins (whose effect is accentuated by the E. coli lipopolysaccharide endotoxin) which lead to the glomerular microangiopathy causing haemolytic uraemic syndrome. Diagnosis is based on identification (monoclonal antibodies, ELISA, PCR) of the verotoxins themselves or the two encoding genes in stool samples. Symptomatic treatment is essential but the effectiveness of antibiotics is still debated. Theoretically, antibiotics could worsen the syndrome by increasing endotoxin release from lysed bacteria, but inversely they could also prevent the syndrome if given early enough. Further research is required to acquire precise epidemiological data and identify animal reservoirs of verotoxin producing E. coli.
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PMID:[Hemolytic-uremic syndrome after verotoxin-producing Escherichia coli infection]. 789 53

Natural killer cell-stimulatory factor or interleukin-12 (NKSF/IL-12) was originally identified and purified from the conditioned medium of Epstein-Barr virus (EBV)-transformed B-cell lines. Phorbol diesters were observed to be potent stimulators of NKSF/IL-12 production from the B-cell lines. Although monocytes were found to be the major producers of NKSF/IL-12 in peripheral blood (PB) in response to lipopolysaccharide (LPS) or to Staphylococcus aureus, several myeloid leukemia cell lines tested did not produce detectable NKSF/IL-12 either constitutively or upon stimulation with phorbol diesters. However, three lines, ML-3, HL-60, and THP-1, responded to LPS with significant levels of NKSF/IL-12 production, whereas S aureus was effective only on THP-1 cells. When the cell lines were preincubated with compounds known to induce them to differentiate, production of tumor necrosis factor alpha (TNF alpha) and IL-1 beta was in most cases maximal in cells with differentiated characteristics, whereas NKSF/IL-12 production in response to LPS in all three producing cell lines was significantly enhanced only by pretreatment with dimethylsulfoxide (DMSO) for 24 hours, or by costimulation with interferon gamma (IFN gamma). The efficiency of DMSO enhancement of NKSF/IL-12 production decreased after 2 to 5 days of incubation, when the cells acquired differentiated characteristics. Unlike DMSO, IFN gamma enhanced NKSF/IL-12 production, and IL-10 and dexamethasone inhibited it in cell lines and PB mononuclear cells stimulated by either LPS or S aureus. The ability of the cell lines to respond to these mediators of possibly physiologically relevant function provides a tissue-culture model for studying their mechanism of action.
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PMID:Differential regulation of interleukin-12 (IL-12), tumor necrosis factor alpha, and IL-1 beta production in human myeloid leukemia cell lines and peripheral blood mononuclear cells. 790 32

The cytokine interleukin-10 (IL-10) has been implicated in the pathogenesis of a number of disease states, including Epstein-Barr virus and human immunodeficiency virus (HIV-1) infections. In the acquired immunodeficiency syndrome (AIDS), it has been suggested that IL-10 may have a deleterious effect by suppressing cell-mediated immunity. However, there are few data on its direct effects on HIV-1 replication. In the present study, we have found that recombinant human IL-10 (rhIL-10), present during days 0 through 2, potently inhibits HIV production in elutriated monocyte/macrophage (M/M) cultures with a 50% inhibitory concentration (IC50) of approximately 0.03 U/mL. This effect did not appear to be caused by toxicity to M/M because there was no change in cell viability, ability to phagocytose latex beads, or protein synthesis as measured by [3H]-leucine incorporation, at doses of rhIL-10 that inhibit viral replication. In addition, lipopolysaccharide-induced production of IL-1 beta, IL-6, or tumor necrosis factor-alpha was not affected at these doses, nor were human mononuclear cell proliferative responses to phytohemagglutinin, OKT3 antibody, or tetanus toxoid. HIV-1 replication was similarly decreased by rhIL-10 in the monocytoid line U937 without signs of cellular toxicity. However, these effects required much higher concentrations of rhIL-10, and viral production was only partially suppressed. rhIL-10 also slightly inhibited HIV-induced cytopathicity in ATH-8, a tetanus toxoid-specific, retrovirally immortalized T-cell line, but had no effect on HIV replication in the H9 and MOLT-4 T cell lines. Thus, rhIL-10 appears to inhibit HIV replication predominantly in cells of the M/M lineage. This effect may serve to reduce viral production in patients with AIDS. However, additional studies will be needed to more precisely define its physiologic role in this disease.
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PMID:Interleukin-10 suppresses human immunodeficiency virus-1 replication in vitro in cells of the monocyte/macrophage lineage. 791 40


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