Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interferon is produced in cultures of rabbit leukocytes in response to infection with Newcastle disease virus or in the absence of known viral infection. The macrophage appears to be the responsible producing cell. Cultures prepared from sterile peritoneal exudates, which contained about 90% macrophages, are at least as efficient as cultures of rabbit kidney (RK) cells in their capacity to synthesize NDV-induced interferon. Interferon can be detected in the medium by 2 hr after viral infection and the titers usually reach a peak of 10,000 PDD(50)/ml by 4-6 hr. Exposure to actinomycin prior to or shortly after viral induction effectively blocks interferon synthesis by cells of both types. However, macrophages become refractory to actinomycin by 30-60 min compared with 607-120 min for RK cells, a finding which suggests earlier and more rapid transcription of interferon-specific messenger RNA in macrophages. Macrophages harvested from the peritioneal cavity of rabbits injected intravenously with NDV 48 hr previously also exhibit slightly reduced capacity to synthesize interferon, but this tolerant state is less marked than is tolerance to production of circulating interferon in intact rabbits. Interferon is also synthesized by rabbit macrophages not infected with virus but simply incubated at 37 degrees C in medium with or without added bacterial endotoxin. Uninfected polymorphonuclear leukocytes, rabbit kidney and spleen cells produced no detectable interferon under similar conditions of cultivation. No interferon was released by intact macrophages incubated at 4 degrees C or by ultrasonically disrupted macrophages incubated at 37 degrees C. Although interferon titers were found to be higher when uninfected cultures were exposed to 10-100 microg/ml of E. coli lipopolysaccharide, unavailability of suitable pyrogen-free maintenance media precluded answering the question whether macrophages can continually synthesize and release interferon spontaneously. Interferon yields from uninfected macrophages were only 1% or less of the yields from NDV-infected macrophages, but the rates of synthesis were similar under both conditions. Studies with actinomycin and puromycin revealed that sequential transcriptive and translational events are required for de novo interferon synthesis by uninfected cells in a manner similar to virus-induced interferon synthesis. The physical properties and molecular weights of these rabbit interferons are discussed in the following report (12).
 ...
PMID:Rabbit macrophage interferons. I. Conditions for biosynthesis by virus-infected and uninfected cells. 416 79

A T cell line was established in long-term tissue culture from spleen cells of BALB/c mice immunized with influenza virus PR8 (A/PR/8/34(H1N1)) by continuous restimulation with PR8 virus and syngeneic x-irradiated spleen cells. This T cell line and clones derived from it have now been propagated for over 1 yr "in vitro". The T cell line and the clones, upon stimulation with Con A in the absence of antigen and irradiated spleen cells, as upon stimulation in the presence of antigen and adherent cells, produce T cell growth factors, B cell replication and maturation factors, and colony-stimulating factors, as tested by restimulation of proliferation of a clone of cytolytic murine T cells, of lipopolysaccharide-activated B cell blasts, and by macrophage/granulocyte colony formation of murine bone marrow cells, respectively. The T cell line and the clones help syngeneic B cells in the presence of syngeneic irradiated spleen cells and PR8 virus to proliferate and mature into clones of cells secreting virus-specific antibodies. In the presence of PR8 virus and of a bystander antigen, such as sheep red cells, B cells specific for this bystander antigen are also induced. Adoptive transfer of the T cells i.v. into syngeneic nu/nu BALB/c mice enable the recipient mice to produce, upon challenge with PR8, virus-specific antibodies and to clear virus infection of the lung. The virus-specific T cell line and the clones are restricted by H-2 antigens of the d-haplotype, probably by Iad, and recognize a determinant on the hemagglutinin (HA) molecule of PR8 virus. Fifty to 100 fmol of virus-associated or free HA suffice for stimulation as measured by proliferation assays. The stimulating determinant is present on the HA of all natural virus isolates of the H1 subtype, is absent from virus isolates of the H2 and H3 subtypes, and is abolished if glutamic acid at position 115 of the HA1 polypeptide of PR8 is replaced by lysine.
 ...
PMID:The recognition specificity of a murine helper T cell for hemagglutinin of influenza virus A/PR/8/34. 618 54

Four procedures were used to evaluate the function of polymorphonuclear leukocytes (PMN) isolated from the blood of cattle experimentally infected with bovine viral diarrhea (BVD) virus: (1) uptake of am emulsion of paraffin oil and Escherichia coli lipopolysaccharide, (2) nitroblue tetrazolium reduction, (3) chemiluminescence, and (4) iodination, or the conversion of iodide to a trichloroacetic acid-precipitable form. A marked impairment of iodination was consistently observed after infection with either a cytopathogenic or a noncytopathogenic strain of BVD virus. A corresponding decrease in paraffin oil uptake, nitroblue tetrazolium reduction, and chemiluminescence was not observed. Serum from BVD virus-infected animals did not depress iodination by normal control PMN in vitro. The iodination, procedure evaluates the activity of the myeloperoxidase, hydrogen peroxide, halide system. This system has potent bactericidal, fungicidal, and virucidal effects. The data indicate that oxidative metabolism by PMN from BVD virus-infected cattle is normal, but that the myeloperoxidase, hydrogen peroxide, halide antibacterial system is impaired. This could be explained by an inhibition of degranulation in PMN from infected cattle. The observed defect in iodination by PMN after BVD virus infection was compounded by a decrease in the number of circulating PMN. The impairment of PMN function may partially explain the increased susceptibility of cattle to secondary bacterial infection during infection with BVD virus.
 ...
PMID:Effects of bovine viral diarrhea virus infection on bovine polymorphonuclear leukocyte function. 626 88

The interplay between feline leukemia virus (FeLV) and feline lymphocytes (lc) infected in vitro or in vivo was investigated. Surface marker analysis and viral infectivity (VI) assays of lc populations were used to determine susceptibility of lc subsets to FeLV. The principal FeLV-replicating cell in the mesenteric lymph node of persistently infected, preleukemic cats was a nonadherent, complement receptor (CR)-bearing lc (B-cell). The lymph nodes of preleukemic cats also had increased numbers of uninfected T-cells [cells forming rosettes with guinea pig erythrocytes (GPE)] and cells with receptors for the Fc portion of 7S IgG (Fc gamma R cells) as compared with lymph nodes of age-matched specific-pathogen-free (SPF) cats. The induction of productive infection of feline peripheral blood mononuclear leukocytes (PBL) in vitro depended on a 48-hour in vitro preincubation period before virus exposure. The equivalent susceptibility of whole and adherent cell-depleted PBL to productive infection and the failure of hydrocortisone to enhance viral infection were compatible with identification of the FeLV-replicating cell as an lc. Furthermore, lc from susceptible SPF kittens replicated 50 times as much FeLV as did lc from resistant adult SPF cats. The Ic productively infected with FeLV after in vitro exposure were more precisely identified with the use of Ficoll-Isopaque density gradient separations of rosetted and nonrosetted lc. Whole PBL, GPE rosette-positive PBL (T-cells), and CR-positive PBL (B-cells) were permissive to FeLV infection, and maximal VI was evident at 14 days after exposure. The substantial (1,325-fold) increment in VI found in the Fc gamma R-depleted PBL suggested a role for Fc gamma R cells in the containment of FeLV infection. Unstimulated mononuclear leukocytes from blood, spleen, lymph node, thymus, and marrow were susceptible to productive FeLV infection after in vitro exposure. The degree of spontaneous DNA synthesis in marrow, thymus, and spleen but not lymph node or PBL was inversely related to permissiveness to viral replication. Mitogen activation of lc was associated with decreased viral replication when either T-cell mitogens (concanavalin A, phytohemagglutinin, or pokeweed mitogen) or a B-cell mitogen (dextran sulfate) was used. Virus production by spleen cells and PBL was enhanced twofold to tenfold by prior lc stimulation by the B-cell mitogen, lipopolysaccharide, or protein A-bearing Staphylococcus aureus, a mitogen for feline T-cells with Fc gamma R. Both productively infected (preincubated) and nonproductively infected (freshly isolated) PBL transferred infectious FeLV to autochthonous peritoneal macrophages (M theta); most of the virus in PBL-peritoneal M theta cocultures was produced by adherent cells, irrespective of whether the adherent or nonadherent cell population was inoculated originally.
 ...
PMID:Determinants of susceptibility and resistance to feline leukemia virus infection. II. Susceptibility of feline lymphocytes to productive feline leukemia virus infection. 626 86

Lipopolysaccharide-responsive C3H/HeN mice were rendered resistant to a mouse-adapted strain of influenza (Aichi, H(3)N(2)) virus when Propionibacterium acnes was given either intranasally or intraperitoneally several days before virus infection. The time of P. acnes treatment was important since no protection was demonstrated when this agent was given either on the same day as or several days after virus challenge. In contrast, lipopolysaccharide-nonresponsive C3H/HeJ mice were not protected when P. acnes was administered intranasally at any time before infection; however, protection was demonstrated when P. acnes was given by the intraperitoneal route. Depending on the route of inoculation, P. acnes induced several distinctive immunological responses in the lungs of both C3H/HeN and C3H/HeJ mice. Intranasal inoculation was more effective in activating pulmonary macrophages in C3H/HeN than in C3H/HeJ mice. In contrast, intraperitoneal inoculation activated pulmonary natural killer cells in both mouse lines but did not activate pulmonary macrophages.
 ...
PMID:Enhancement of natural resistance to influenza virus in lipopolysaccharide-responsive and -nonresponsive mice by Propionibacterium acnes. 683 17

Aged mice of the CBA/Ca strain, 15 months of age, and A/J mice, 17 months of age, exhibited impaired lymphoblastogenic response to concanavalin A but not to lipopolysaccharide. This defective cellular responsiveness was not accompanied by decreased antibody response to protein antigen or decreased ability to develop delayed hypersensitivity to picryl chloride. An increased susceptibility to influenza virus infection given intranasally was noted in the aged mice as compared with young animals. Such virus infection also impaired the lymphoblastogenic response to mitogens. Surprisingly, the virus infection in aged animals was less lethal after a subsequent infection with a small inoculum of Listeria bacteria.
 ...
PMID:Protective effect of sublethal intraperitoneal Listeria infection secondary to intranasal influenza infection in aged immunodeficient mice. 719 67

Passively acquired immunity to herpes simplex virus (HSV) was studied in antithymocyte serum (ATS)-treated mice and athymic nude mice to determine whether immunocompetent lymphocytes contribute to the protection observed after transfer of HSV-specific antibody to infected animals. Mice were given three intraperitoneal injections of 0.1 ml of ATS at 24-h intervals. This treatment reduced concanavalin A and lipopolysaccharide stimulation of lymphocytes harvested from these animals by 90% when compared with the stimulation of lymphocytes harvested from untreated animals. It was found that intraperitoneal injection of 0.5 ml of specific antibody 8 h after corneal HSV type 1 infection or subcutaneous HSV type 2 infection did not protect ATS-treated animals from virus infection. Specific antibody passively transferred to ATS-treated animals 8 and 120 h postinfection also failed to protect lymphocyte-depleted animals from HSV. However, ATS-treated animals were protected from HSV infection by passively acquired antibody when lymphocytes harvested from these animals regained 80% of their ability to be stimulated with concanavalin A and lipopolysaccharide. It was also found that specific antibody conferred protection to nude mice infected with HSV only if they were first reconstituted with syngeneic thymus cells 48 h before infection. The results suggest that both antiviral antibody and thymus-derived lymphocytes contribute to the recovery of HSV-infected hosts after passive immunization.
 ...
PMID:Lymphocyte reactivity contributes to protection conferred by specific antibody passively transferred to herpes simplex virus-infected mice. 721 31

Nine of seventeen neonatal Holstein-Friesian calves were thymectomized, treated with antilymphocyte globulin, and monitored for immunologic functional ability for 4 to 6 months. The thymus weights for 4 to 10-day-old calves and 4 to 6-month-old calves indicated a continued increase in total weight. This indicated significant thymic involution had not occurred at 4 to 6 months. Following thymectomy a wasting syndrome was not observed although an increased incidence of a lowly virulent virus infection did occur. A significant decrease in circulating lymphocytes was observed. Peripheral blood lymphocytes were stimulated in vitro by non-specific mitogens, phytohemagglutinin, bacterial lipopolysaccharide and pokeweed mitogen using the whole blood culture method. Observations included a greater response to phytohemagglutinin and pokeweed mitogen in summer months and variable age related response to all mitogens. Lipopolysaccharide stimulation results were inconclusive. It was concluded that neonatal thymectomy was not a satisfactory experimental procedure for the production of selective immunosuppression in the bovine species.
 ...
PMID:Effect of neonatal thymectomy and antilymphocyte globulin on non-specific mitogen stimulation in Holstein-Friesian calves. 734 68

To examine the in vivo role(s) of type I interferons (IFNs) and to determine the role of a component of the type I IFN receptor (IFNAR1) in mediating responses to these IFNs, we generated mice with a null mutation (-/-) in the IFNAR1 gene. Despite compelling evidence for modulation of cell proliferation and differentiation by type I IFNs, there were no gross signs of abnormal fetal development or morphological changes in adult IFNAR1-/- mice. However, abnormalities of hemopoietic cells were detected in IFNAR1 -/- mice. Elevated levels of myeloid lineage cells were detected in peripheral blood and bone marrow by staining with Mac-1 and Gr-1 antibodies. Furthermore, bone marrow macrophages from IFNAR1 -/- mice showed abnormal responses to colony-stimulating factor 1 and lipopolysaccharide. IFNAR1 -/- mice were highly susceptible to viral infection: viral titers were undetected 24 hr after infection of IFNAR1 +/+ mice but were extremely high in organs of IFNAR1 -/- mice, demonstrating that the type I IFN system is a major acute antiviral defence. In cell lines derived from IFNAR1 -/- mice, there was no signaling in response to IFN-alpha or -beta as measured by induction of 2'-5' oligoadenylate synthetase, antiviral, or antiproliferative responses. Importantly, these studies demonstrate that type I IFNs function in the development and responses of myeloid lineage cells, particularly macrophages, and that the IFNAR1 receptor component is essential for antiproliferative and antiviral responses to IFN-alpha and -beta.
 ...
PMID:A null mutation in the gene encoding a type I interferon receptor component eliminates antiproliferative and antiviral responses to interferons alpha and beta and alters macrophage responses. 747 80

Apoptosis plays an important role in generating and maintaining an effective immune system. Many pathogens can perturb the homeostasis of the immune system by either inducing or suppressing cell death of immune cells. Using bovine macrophages as a model, we found that interferon-alpha, one of the host's responses to viral infection, can prime macrophages for activation-induced apoptosis. Exposure of bovine bone-marrow-derived macrophages to interferon-alpha and subsequent activation with lipopolysaccharide led to a strong downregulation of the macrophages' nitric oxide production when compared to lipopolysaccharide stimulation alone. We could show that this was due to induction of apoptosis after activation of the cells. Herpesvirus-induced type I interferon also primed bovine macrophages for lipopolysaccharide-induced apoptosis. Our studies describe how in a novel pathway an antiviral immune response could contribute to pathological sequelae of viral diseases.
 ...
PMID:Interferon-alpha primes macrophages for lipopolysaccharide-induced apoptosis. 748 62


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>