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)

It was hypothesized that the generation of activated T cells through an efficient and rapid immune response during the early pathogenesis of Marek's disease virus (MDV) infection provides a large pool of target cells for transformation. Therefore, the correlation between genetic susceptibility to Marek's disease (MD) and in vitro mitogenic responses of lymphocytes as a measure of cell-mediated immune competence and efficiency was tested. In one series of trials, spleen cells from strains of chickens with differing levels of susceptibility to MD tumors were stimulated with graded doses of Concanavalin A (Con A) or phytohemagglutin (PHA). In a second series of trials, peripheral blood lymphocytes from individual chickens within genetic strains were tested at the same time chickens were challenged with MDV to determine susceptibility. Responsiveness was determined using one-way mixed lymphocyte reaction (MLR) tests as well as mitogen stimulation. Data from the tests comparing chicken strains supported the hypothesis in some but not all cases. The S13 chickens, which are more susceptible than P2a chickens to MD, were significantly more responsive, and highly resistant N2a chickens were significantly less responsive to Con A. In contrast, five other resistant strains were either more responsive (UCD-058, OS13) or equally responsive (UCD-140, OS5, C) to Con A when compared with P2a chickens. The PHA responses were even less predictive of MD susceptibility. No general correlation was observed between responsiveness to either mitogen or MLR tests and subsequent tumor development in trials comparing individuals within strains.
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PMID:Immune response versus susceptibility to Marek's disease. 278 54

Three pairs of chicken lines selected for high (H) and low (L) graft vs. host reaction (GVHR) competences, serum immunoglobulin G (IgG) levels, and antibody responses to Leucocytozoon caulleryi were examined for their immunocompetences and Marek's disease (MD) resistance. The GVHR-H and GVHR-L lines were further divided into two sublines according to their major histocompatibility B genotype. Immune responses to sheep erythrocytes (SRBC), bovine serum albumin (BSA), and a lipopolysaccharide (LPS) were compared between the high and low lines of each pair of selected lines. Significant differences were found in responses to SRBC and LPS in IgG-selected lines and in response to BSA in Leucocytozoon-selected lines. In all three instances antibody titers of the H line were higher than those of the L line. The GVHR competence expressed by the splenomegaly index (SI) was also significantly different between the H and L lines of all three selected-line pairs. The SI values in the GVHR-selected and IgG-selected lines were higher in the H line than in the L line, whereas those in the Leucocytozoon-selected lines were lower in the H line. Differences in MD incidence and in MD mortality were found between the GVHR-selected B11B11 subline and the IgG-selected lines. In both instances the L line was more resistant to MD than the H line.
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PMID:Immunocompetences and Marek's disease resistance in three pairs of chicken lines selected for different immunological characters. 362 59

The replication of Marek's disease herpesvirus (MDV) and herpesvirus of turkeys (HVT) in chicken embryo fibroblast (CEF) cultures was inhibited by the addition of S-nitroso-N-acetylpenicillamine, a nitric oxide (NO)-generating compound, in a dose-dependent manner. Treatment of CEF culture, prepared from 11-day-old embryos, with recombinant chicken gamma interferon (rChIFN-gamma) and lipopolysaccharide (LPS) resulted in production of NO which was suppressed by the addition of N(G)-monomethyl L-arginine (NMMA), an inhibitor of inducible NO synthase (iNOS). Incubation of CEF cultures for 72 h prior to treatment with rChIFN-gamma plus LPS was required for optimal NO production. Significant differences in NO production were observed in CEF derived from MDV-resistant N2a (major histocompatibility complex [MHC], B(21)B(21)) and MDV-susceptible S(13) (MHC, B(13)B(13)) and P2a (MHC, B(19)B(19)) chickens. N2a-derived CEF produced NO earlier and at higher levels than CEF from the other two lines. The lowest production of NO was detected in P2a-derived CEF. NO production in chicken splenocyte cultures followed a similar pattern, with the highest levels of NO produced in cultures from N2a chickens and the lowest levels produced in cultures from P2a chickens. Replication of MDV and HVT was significantly inhibited in CEF cultures treated with rChIFN-gamma plus LPS and producing NO. The addition of NMMA to CEF treated with rChIFN-gamma plus LPS reduced the inhibition. MDV infection of chickens treated with S-methylisothiourea, an inhibitor of iNOS, resulted in increased virus load compared to nontreated chickens. These results suggest that NO may play an important role in control of MDV replication in vivo.
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PMID:Inhibitory effects of nitric oxide and gamma interferon on in vitro and in vivo replication of Marek's disease virus. 1072 36

The role of cytokines in the pathogenesis and immunity of Marek's disease (MD), a herpesvirus-induced T-cell lymphoma in chickens, is poorly understood. Two different experiments were used to examine the potential role of particular cytokines in the pathogenesis and immune responses of MD. First, chicken embryo fibroblasts (CEF) were stimulated with lipopolysaccharide (LPS) and/or recombinant chicken interferon-gamma (rChIFN-gamma) and used to develop techniques for examining transcription of IFN-alpha, IFN-gamma, inducible nitric oxide synthase (iNOS), interleukin (IL)-1beta, IL-2, IL-6 and IL-8 by reverse transcription-polymerase chain reaction (RT-PCR). Addition of LPS and/or rChIFN-gamma resulted in the up-regulation of mRNA for iNOS, IL-1beta and IL-6, while IFN-gamma was up-regulated by LPS alone. IL-2 was down-regulated by the treatments. Second, to determine the effects of Marek's disease herpesvirus (MDV) infection on cytokine transcription in vivo, chickens were infected with MDV at 21 days of age and examined at 7 days post-infection (p.i.) (exp. 1) or were infected with MDV at 1 day of age and examined from 3 to 15 days p.i. (exp. 2). In MDV-infected chickens, IFN-gamma transcription was up-regulated as early as 3 days p.i. until the termination of the experiment at 15 days p.i., while iNOS and IL-1beta were up-regulated between 6 and 15 days p.i. Infection of 1-day-old chicks increased levels of mRNA for IFN-gamma and iNOS between 16- and 64-fold at 9 days p.i. These results suggest that IFN-gamma and iNOS may play an important role in the pathogenesis of MD.
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PMID:Expression of cytokine genes in Marek's disease virus-infected chickens and chicken embryo fibroblast cultures. 1080 61

Nitric oxide (NO), a free radical produced by the enzyme NO synthase (NOS), is a potent antiviral agent in addition to having immune regulating functions. Recently, it was reported that chickens resistant (N2a, MHC: B21B21) to the development of Marek's disease (MD) had a greater potential to produce NO than MD-susceptible chickens (P2a, MHC: B19B19). This difference was shown by measuring NO levels in chick embryo fibroblast cultures obtained from these chickens after treatment with lipopolysaccharide and recombinant chicken interferon-gamma (IFN-gamma). To extend these results, the levels of NO in blood plasma from N2a and P2a chickens inoculated with the nonattenuated JM-16 strain of MD virus (MDV) were examined. In four out of five experiments, N2a chickens had increased NO levels at 7 days postinoculation (DPI). In contrast, P2a chickens challenged with JM-16 had a significant increase in NO in only one of four experiments, and in that experiment the increase was delayed (10 DPI) compared with N2a chickens. Attenuation abrogated MDV-induced NO in chickens. Inoculation with MDV strains ranging from mild to very virulent plus showed that the more virulent strains induced the highest level of NO in blood plasma, suggesting a role of NO in the pathogenesis of MD with more virulent strains. On the basis of quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) assays for analysis of mRNA expression, IFN-gamma does not appear to be the primary inducer of inducible (i)NOS gene expression during MDV infection. iNOS gene expression and NO production are mediated during the cytolytic phase of MDV infection on the basis of real-time RT-PCR assays with primers specific for glycoprotein B, a late gene expressed only during the cytolytic phase of MDV infection. These findings implicate NO as a factor potentially involved in increasing virulence of MDV, possibly through immune suppression.
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PMID:Influence of genetic resistance of the chicken and virulence of Marek's disease virus (MDV) on nitric oxide responses after MDV infection. 1224 28

We describe the characterization of a spontaneously transformed chicken monocytic cell line that developed as a single colony of cells in a heterophil culture that was inadvertently left in the incubator over a period of 25 days. These cells, hitherto named HTC, grow efficiently at both 37 or 41 degrees C in culture medium containing either 5% FBS or 2% chicken serum. The HTC cells are acid phosphatase positive, show expressions of both class I and class II major histocompatibility complex (MHC), CD44, K1, and K55 cell surface antigens, and engulf latex beads, produce nitrite and interleukin-6 on stimulation with bacterial lipopolysaccharide (LPS). Treatment with phorbol myristate acetate (PMA) induces respiratory burst in HTC cells and the secretion of matrix metalloproteinase (MMP) into culture medium. Using gene-specific primers and reverse transcriptase-polymerase chain reaction (RT-PCR), the presence of mRNA trancripts for interferon-gamma (IFN-gamma), interleukin-1 (IL-1), interleukin-6 (IL-6), nitric oxide synthase (NOS), matrix metalloproteinase-2 (MMP-2), and transforming growth factor-beta (TGF-beta) were detected. Lipopolysaccharide (LPS) treatment of HTC cells modulated IL-1, IL-6, IFN-gamma, NOS mRNA levels as detected by RT-PCR analyses. Using different avian tumor virus gene-specific primers and PCR, the HTC cells were positive for the presence of avian leukosis virus (ALV) and Marek's disease virus (MDV) but negative for reticuloendothelial virus (REV), chicken infectious anemia virus (CIAV), and herpes virus of turkeys (HVT). The production of ALV antigens by HTC cells was further confirmed using p27 gag protein ELISA. Collectively, these results show that the HTC cells belong to myeloid/macrophage lineage and were likely transformed by ALV and MDV but retain many interesting and useful biological activities.
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PMID:Characterization of a spontaneously transformed chicken mononuclear cell line. 1452 38

Studies have been performed on the induction of cytostatic activity of cultured chicken bone-marrow-derived macrophages. Cultured macrophages were exposed to supernatants of ConA-stimulated spleen cell cultures (lymphokines), lipopolysaccharide (LPS), ConA or infectious bursal disease virus (IBDV). Cytostatic activity of macrophages was examined by testing their growth-inhibiting effect on T-lymphoblastoid Marek's disease cell lines RP-1, HP-2 and MSB-1 as target cells. Lymphokines, LPS and IBDV caused considerable enlargement of adherent macrophages. Results of cytostasis assays suggested that morphological signs of macrophage activation were not correlated with the cytostatic potency of activated macrophages. Lymphokine-activated macrophages caused at least an 80% growth inhibition of target cells, whereas LPS, ConA or IBDV-activated macrophages exhibited only a marginal cytostatic effect in the range of 20%. Attempts to detect soluble cytostatic factors in supernatants of activated macrophage cultures failed or had equivocal results. Untreated macrophages were rarely cytostatic at an effector:target cell ratio of I:1 to 4:1, and they stimulated RP-1 cell growth if these cells were seeded at suboptimal concentrations. The results suggest that the suppressor activity of macrophages from Marek's disease virus-infected chickens, as demonstrated by other authors in vitro, is probably a result of nonspecific immunomodulation in vivo where lymphokines may also play a major role.
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PMID:Growth inhibition of Marek's disease T-lymphoblastoid cell lines by chicken bone-marrow-derived macrophages activated in vitro. 1876 75

Studies have been made with the immunosuppressive drug cyclosporin A (CsA) to examine its value in the establishment of lymphoid tumour cell lines from Marek's disease (MD) lymphomas and from lymphoid cell cultures exposed to MD virus in vitro. CsA was shown to depress the proliferative response of normal spleen cells to phytohaemagglutinin, Concanavalin A and pokeweed mitogen, and to a lesser extent to lipopolysaccharide. Short-term proliferative responses of lymphoma cells were either not affected, depressed or stimulated by CsA. The efficiency of establishment of lymphoid cell lines from long-term cultures of lymphoma cells was not increased by CsA, and the drug had a depressive effect on the proliferation of cell lines in the lympho-cytoid stage. The majority of lymphoblastoid cell lines studied were stimulated by CsA. Interleukin 2 partially overcame the suppressive effect of CsA on the cell lines, and enhanced the stimulatory effects. Cultures of lymphoid cells exposed to MD virus in vitro were usually depressed by CsA; a few stimulatory combinations were observed, but these were not considered to be of biological significance. These results indicate that CsA suppresses normal T-cell responses in the chicken, but that some MD-associated lymphoid cells are stimulated by the drug, in some instances at least by a direct effect.
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PMID:Effect of cyclosporin a on normal, mitogen-stimulated and Marek's disease virus-exposed and transformed chicken lymphoid cells. 1876 2

Two primary broiler breeder lines, A and B, were examined for their potential to produce nitric oxide (NO) after stimulating splenocytes from 20-day-old embryos with lipopolysaccharide and interferon-gamma. Significant differences were found between lines A and B. Overall, line A had a higher response than line B, but line A also had a large degree of variation between individual sire families. Selection for high and low responders within line A resulted in the segregation of high- and low-responder sire families. Offspring from sire families selected for high and low NO responses and from a nonselected control group from line A were challenged with RB-1B Marek's disease (MD) virus to determine whether these differences could be used to select for improved resistance to MD. Virus isolation rates at 6 and 10 days postinfection were not significantly different, but unexpectedly, the MD incidence in the high-responder group was significantly higher than in the other two groups.
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PMID:Selection for increased nitric oxide production does not increase resistance to Marek's disease in a primary broiler breeder line. 1984 69

Ligands for Toll-like receptors (TLRs) are known to stimulate immune responses, leading to protection against bacterial and viral pathogens. Here, we aimed to examine the effects of various TLR ligands on the development of Marek's disease in chickens. Specific-pathogen free chickens were treated with a series of TLR ligands that interact with TLR3, TLR9 and TLR21. In a pilot study, it was determined that TLR4 and TLR21 ligands are efficacious, in that they could reduce the incidence of Marek's disease tumors in infected birds. Hence, in a subsequent study, chickens were treated with lipopolysaccharide (LPS) as a TLR4 and CpG oligodeoxynucleotides (ODN) as TLR21 agonists before being challenged with the RB1B strain of Marek's disease virus (MDV) via the respiratory route. The results demonstrated that the administration of LPS or CpG ODN, but not PBS or non-CpG ODN, delayed disease onset and reduced MDV genome copy number in the spleens of infected chickens. Taken together, our data demonstrate that TLR4 and 21 agonists modulate anti-virus innate immunity including cytokine responses in MD-infected chicken and this response can only delay, but not inhibit, disease progression.
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PMID:The effects of administration of ligands for Toll-like receptor 4 and 21 against Marek's disease in chickens. 2453 Sep 27


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