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)

African swine fever virus infected most, if not all, of the macrophages (monocytes) and ca. 4% of the polymorphonuclear leukocytes from porcine peripheral blood. B and T lymphocytes, either resting or stimulated with phytohemagglutinin, lipopolysaccharide, or pokeweed mitogen, were not susceptible to the virus. All of the mitogens used inhibited African swine fever multiplication in susceptible cells. The number of virus passages in vitro and the virulence degree of the virus did not affect the susceptibility of porcine B or T lymphocytes to African swine fever virus.
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PMID:Porcine leukocyte cellular subsets sensitive to African swine fever virus in vitro. 638 55

CD69 is an early marker of lymphoid cell activation. The authors report on an up-regulation of CD69 in splenic B and T cells of C57Bl/6 mice after administration of lipopolysaccharide (LPS) or microbial immunosuppressive/mitogenic (ISM) proteins produced by C. albicans (p43) and African Swine Fever Virus (p36). This up-regulation of CD69 was observed 6 and 24 h after mitogenic treatments. The same pattern of increased CD69 expression was observed in the lymph nodes of mice treated with p43 or LPS, whereas p36 treatment failed to induce increased CD69 expression in this organ. Intracellular calcium mobilization was induced in splenic B and T lymphocytes after incubation of total spleen cells with LPS, p43 or p36. This increase was higher in B than in T cells. Increased calcium mobilization was also seen in lymph node B cells after incubation with p43 or p36 and in lymph node T cells after p43 stimulation. Up-regulation of CD69 expression on B and T cells was also observed after in vitro stimulation of spleen cells with the three mitogens used. Similar results were obtained with culture supernatants of macrophage/monocyte (M phi) cells activated with LPS (LPS/M phi CS). Stimulation of M phi cells with LPS or with the ISM proteins is demonstrated by the increased production of nitrites by these cells. The increased in vitro expression of CD69 was, however, not abolished by monoclonal antibodies to M phi cytokines such as IL-6, IL-10 or TNF alpha. No increased expression of CD69 was found in vitro on purified B or T cells, even when mixed upon stimulation with p43, p36, LPS or with LPS/M phi CS. However, an increase in the expression of CD69 was observed on B cells co-cultured with M phi cells after treatment with LPS or p36. All three mitogens failed to induce increased CD69 expression on cultured T cells mixed with M phi cells.
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PMID:Role of monocytes in the up-regulation of the early activation marker CD69 on B and T murine lymphocytes induced by microbial mitogens. 863 95

Cytokines produced by cells of the immune system, including macrophages, can influence inflammatory responses to viral infection. This has been exploited by viruses, which have developed strategies to direct the immune response towards ineffective responses. African swine fever virus (ASFV) is a double-stranded DNA virus that infects macrophages of domestic swine. In this study, primary cells of monocyte macrophage lineage were obtained from the lungs, peritoneum or blood of domestic swine and, after infection with ASFV, supernatants were tested for cytokines using biological assays. The cytokine transforming growth factor-beta (TGF-beta) was detected after infection of macrophage preparations, but tumour necrosis factor (TNF) and interleukin-1 (IL-1) were not detected. ASFV-infected and uninfected macrophage populations were also tested to assess their ability to respond to cytokines by enhancing production of superoxide in the respiratory burst mechanism. Responses to interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS) were suppressed in macrophage populations infected with virus, even at low multiplicities of infection. Addition of TGF-beta to uninfected macrophages resulted in a similar suppression of response, but antibody to TGF-beta did not prevent suppression induced by virus. These results are discussed in relation to the pathology of African swine fever.
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PMID:Changes in swine macrophage phenotype after infection with African swine fever virus: cytokine production and responsiveness to interferon-gamma and lipopolysaccharide. 930 35

Cultured mammalian cells are traditionally maintained at 37 degrees C, despite the fact that core body temperatures differ considerably among mammals. Considering the body temperature of the adult pig, comparison was made of porcine macrophage cultures maintained at 37 degrees C and 39.2 degrees C. Examination of the cells showed that granularity was higher in macrophages maintained at 39.2 degrees C, although no differences in cell size were observed. The density of MHC Class I and II expression was higher on cells maintained at 39.2 degrees C, as was the percentage of MHC Class II positive cells. In contrast, expression of CD44 and CD11a/18 remained unchanged. Following stimulation with lipopolysaccharide, only cells maintained at 39.2 degrees C produced detectable levels of TNF-alpha. As a final reference criterion, replication of the macrophage tropic African swine fever virus was monitored. At 39.2 degrees C, virus antigen production was less efficient, and virus isolate-related differences in the replication kinetics were observed. Infectious virus production was not different at the two temperatures, implying that virus maturation may have been more efficient at the higher temperature. These results indicate that incubation of cultured cells at the temperature of their donor species has an important influence on their characteristics.
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PMID:Macrophage culture: influence of species-specific incubation temperature. 969 68

Uncontrolled generation of nitric oxide (NO) by inducible nitric-oxide synthase (iNOS) can cause damage to host cells and inflammation, two undesirable events for virus spreading. African swine fever virus (ASFV) infection regulates iNOS-induced gene expression through the synthesis of the A238L virus protein. We here explored the role of A238L, an NF-kappaB and NFAT inhibitor, in the regulation of iNOS transcription in macrophages. NO production and iNOS mRNA and protein levels as well as iNOS promoter activity after lipopolysaccharide (LPS)-gamma interferon (IFN-gamma) treatment were down-regulated both during ASFV infection and in Raw 264.7 cells stably expressing the viral protein. Overexpression of p300, but not of a histone acetyltransferase (HAT) defective mutant, reverted the A238L-mediated inhibition of both basal and LPS-IFN-gamma-induced iNOS promoter activity. Following stimulation with LPS-IFN-gamma, p65 and p300 interaction was abolished in Raw-A238L cells. Expression of A238L also inhibited p65/relA and p300 binding to the distal NF-kappaB sequence of the iNOS promoter together with p65 acetylation. Finally, A238L abrogated p300 transactivation mediated by a GAL4-p300 construction. These results provide evidence for an unique viral mechanism involved in transcriptional regulation of iNOS gene expression.
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PMID:Regulation of inducible nitric oxide synthase expression by viral A238L-mediated inhibition of p65/RelA acetylation and p300 transactivation. 1704 Dec 21