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PubMed1979

Immune responses in mice infected with lactic dehydrogenase virus. IV. Functional status of the macrophage during acute LDV infection.

Macrophages from uninfected and lactic dehydrogenase virus (LDV)-infected mice were compared with respect to the affinity and number of their Fc receptors for IgG2a; no differences were found regarding these parameters. When the uptake of DNP-BGG by macrophages from uninfected and acutely LDV-infected mice was compared, again no differences were observed. However, when the per cent membrane-bound DNP-BGG was determined as a function of time after antigen uptake in these two groups, more DNP-BGG was found membrane-bound on the macrophages from the LDV-infected mice, than on uninfected macrophages. In view of the fact that humoral immunity is enhanced during acute LDV infection, these data provide a positive correlation between increased retention of membrane-bound antigen and enhanced humoral immune responses.

Acute Disease↗
PubMed1977

Immune responses in mice infected with lactic dehydrogenase virus. I. Antibody response to DNP-BGG and hyperglobulinaemia in BALB/c mice.

The humoral immune response to DNP-BGG of BALB/c mice acutely infected with lactic dehydrogenase virus (LDV) has been investigated. Virus-infected mice injected with antigen in saline exhibit a greater anti-DNP response than uninfected controls. When this antigen is presented in Freund's complete adjuvant (FCA) the anti-DNP response is greater than obtained with antigen in saline, but significant differences between infected and uninfected controls are not observed. These data are consistent with the view that acute LDV infection can have an adjuvant-like effect when this T-dependent antigen is introduced in saline. In addition, the effect of viral infection on plasma Ig class and subclass levels has been investigated. LDV infection leads to a gradual increase in plasma Ig concentration. This effect is restricted to the IgG2a subclass in most animals, but occasionally is restricted to IgG1. The mechanisms responsible for these changes have not been delineated.

Adjuvants, Immunologic↗
PubMed1978

Lactic dehydrogenase virus alteration of lymphocyte circulation.

Acute infection with lactic dehydrogenase virus (LDV) causes a systemic alteration in lymphocyte circulatory patterns. Peripheral lymph nodes (LN) and spleens in acutely, but not chronically, infected mice retain a significantly greater proportion of injected 51Cr-labeled lymphocytes than the respective tissues in noninfected controls. This increase in lymphocyte localization in LN and spleen is dependent upon the dose of LDV injected and the timing of the infection. A relatively large dose of LDV (10(8) infectious units) causes an early but very transient increase in splenic lymphocyte localization accompanied by an early but prolonged increase in lymphocyte recovery in LN. Smaller doses of LDV cause more prolonged effects on splenic lymphocyte recovery and retarded effects on lymphocyte localization in LN. Increases in splenic recovery were always accompanied by decreases in hepatic recovery of lymphocytes. LDV-induced alteration in lymphocyte circulation may be responsible for many previously observed modifications of immune responses in LDV-infected mice.

Animals↗
PubMed1992

Lactic dehydrogenase virus infection prevents development of anti-nuclear antibody in (NZB x NZW)F1 mice; role of prostaglandin E2 and macrophage Ia antigen expression.

Persistent lactic dehydrogenase virus (LDV) infection prevents the development of antinuclear antibody (ANA) in (NZB x NZW)F1 mice. To assess the suppressive mechanisms, we focused on the role of the E series of prostaglandin(PGE), since previously we have shown enhanced production of PGE by macrophages from chronically LDV-infected mice. Treatment with PGE2 suppressed ANA titres more markedly in non-infected mice than in LDV-infected mice. Indomethacin enhanced ANA titres more markedly in LDV-infected mice than in non-infected mice. The number of Ia antigen positive(Ia+) macrophages was less in LDV-infected mice than in uninfected mice. The number of Ia+ macrophages was decreased in non-infected mice by PGE2 treatment and increased in LDV-infected mice by indomethacin treatment. These results suggest that the low ANA production in LDV-infected (NZB x NZW)F1 mice may be related to the decreased number of Ia+ macrophages and that one of the factors responsible for suppression of Ia+ macrophages may be the enhanced PGE2 production in the LDV-infected mice.

Animals↗
PubMed1992

Suppression of development of diabetes in NOD mice by lactate dehydrogenase virus infection.

It has been reported that lactate dehydrogenase virus (LDV) selectively infects a subpopulation of macrophages, thereby affecting the immune system. We studied the effects of LDV infection on the development of diabetes in non-obese diabetic (NOD) mice. Five-week-old female NOD mice were infected with LDV (10(8) ID50/mouse) and observed until 23 weeks of age. None of the 21-LDV-infected mice developed diabetes, whereas 10/14 (71.4%) uninfected mice did. Although the subpopulations of T cells and the percentage of Mac1-positive cells in the NOD murine spleen and the number of harvested peritoneal macrophages were unaffected by LDV infection, the proportions of Ia-positive peritoneal macrophages were significantly decreased in LDV-infected compared with uninfected mice (1.1 +/- 0.2%, 6.5 +/- 2.9%; P < 0.01). In LDV-infected NOD mice, insulitis of the same grade as that seen in uninfected NOD mice was observed. In another experiment, 3, 5, 10 or 16-week-old female NOD mice were infected with LDV. None of the mice infected with LDV at 3, 5 or 10 weeks of age developed diabetes and only one of six infected at 16 weeks of age did. These findings indicate that LDV infection suppresses the development of diabetes in female NOD mice by reducing the capacity of Ia-positive macrophages, and suggest that the development of human type 1 diabetes may be suppressed by certain viral infections.

Animals↗
PubMed1975

Distribution along the axon and into various subcellular fractions of molecules labeled with (3H)leucine and rapidly transported in the garfish olfactory nerve.

The distribution of molecules labeled with [3H]leucine by fast axoplasmic transport in vivo has been studied in the garfish olfactory nerve after incorporation of the amino acid by the olfactory mucosa. Owing to the size of the nerve, it has been possible to follow the fate of the labeled molecules in 10 different subcellular fractions of 6 consecutive nerve segments. Each segment represents a different part of the profile developed by the transported radioactive molecules. In order to determine the influence of the perikaryon (rate of protein synthesis and rate of protein release into the axon) transport was studied under 3 different conditions: (1) intact nerves (simply labeled with [3H]leucine); (2) nerves cut from the cell bodies 6 h after application of [3H]leucine; and (3) nerves pulse-chase labeled for 1 h. Several conclusions can be drawn. (1) The bulk of the rapidly transported molecules are membranous axonal proteins, as determined by enzyme markers. Most are found in subcellular fractions representing 17% of the total axonal protein. They are synthesized very rapidly in the cell bodies (less than 1 h after isotope deposition) and exhibit the highest specific activities measured. These high specific activities were found in the same axonal membrane fractions in both plateau and crest, suggesting that the membrane precursors are transported as particles rather than as subunits. (2) The majority of these proteins are released into the axon immediately after synthesis; however, at least 30% of the labeled axonal membranous proteins are not released with the fast wave itself but progressively over a long period of time. (3) The majority of the moving material, particularly in membranous fractions, is left behind the fast wave and is deposited in the axon. When the front base of the fast wve has covered 70% of the total nerve length, only 19% of the labeled material of the main axonal membranous fraction appears still to be moving. (4) Proteins with high specific activities are found near the cell bodies and may be the result of early axonal transport of amino acids, diffusing later into the surrounding cells and being incorporated into proteins. Some free amino acids are also transported along the axon.

Acetylcholinesterase↗
PubMed1992

Effect of prostaglandin E2 on plasma lactic dehydrogenase activity in (NZB x NZW)F1 mice with a chronic infection of lactic dehydrogenase virus.

The effect of prostaglandin E2(PGE2) on blood LDH values was investigated in (NZB x NZW)F1 mice with or without an established infection with lactic dehydrogenase virus (LDV). Plasma LDH decreased in infected mice treated with PGE2, but increased in infected mice treated with indomethacin, an inhibitor of PGE2. However no significant effect on LDH occurred in uninfected mice treated with PGE2 or indomethacin. To investigate the mechanisms of decreased LDH activities resulting from treatment with PGE2, clearance tests were performed. Clearance of LDH-5, but not LDH-1, was faster in PGE2-treated mice than in non-treated mice, whether or not they were infected with LDV. The results suggest that enhanced clearance of LDH-5 in mice treated with PGE2 may account for the fall in plasma LDH in LDV-infected mice.

Animals↗
PubMed1992

Enhanced clearance of lactic dehydrogenase-5 in severe combined immunodeficiency (SCID) mice: effect of lactic dehydrogenase virus on enzyme clearance.

The lactic dehydrogenase (LDH) level in plasma and the clearance of LDH in C.B-17 scid (severe combined immunodeficiency; SCID) mice were compared with those in C.B-17 or BALB/cCrSlc mice with or without lactic dehydrogenase virus (LDV) infection. The resting enzyme level in SCID mice showed little difference from that in C.B-17 or BALB/cCrSlc mice. The degree of increased plasma LDH level in SCID mice was lower than that in C.B-17 and BALB/cCrSlc mice after LDV infection. To assess the mechanisms of decrease in LDH elevation in SCID mice infected with LDV, virus replication was compared in SCID and BALB/cCrSlc mice. The infectivity titre of plasma in SCID mice was higher (more than 10 times) than that in BALB/cCrSlc mice. Moreover, the percentage of virus antigen positive Kupffer cells was higher in SCID mice than that in BALB/cCrSlc mice. The level of endogenous LDH release as a result of carbon tetrachloride treatment was similar in the SCID and BALB/cCrSlc mice. The clearance rate of endogenous LDH was greater in SCID mice than in BALB/cCrSlc mice with or without LDV infection. The rate of clearance of intravenously injected porcine LDH-5, but not porcine LDH-1, was enhanced in SCID mice as compared with that in BALB/cCrSlc mice. Furthermore, carbon clearance was higher in SCID mice than that in BALB/cCrSlc mice. These results suggest that the smaller increase of plasma LDH after infection might be due, at least in part, to the enhanced LDH-5 clearance function by macrophages in SCID mice.

Animals↗
PubMed1979

Matching of chemotherapy to mouse strain and lymphoid tumor type to prevent tumor-induced suppression of specific T- and B-cell functions.

Specific immunological and hematopoietic functions were studied during treatment with antineoplastic agents in mice bearing syngeneic lymphoid tumors: 70Z/2, a B-cell lymphoma of C57BL X DBA/2 F1 (hereafter called (BD2F1) mice; EL4, a T-cell lymphoma of C57BL/6 mice; or J774, a macrophage tumor of BALB/c mice. Both B- and T-lymphocyte function (antibody-forming cells and cell-mediated lymphocyte lympholysis toward alloantigens) were suppressed in spleen cells of mice bearing these tumors. Other hematopoietic functions (granulocyte, macrophage, and megakaryocyte progenitor cells) were variably influenced by growth of these lymphoid tumors. J774 enhanced, but 70Z/2 suppressed, megakaryocyte progenitor cells. J774 and 70Z/2 increased levels of granulocyte-macrophage progenitor cells. EL4, the T-cell lymphoma, did not influence either cell type. Significant variation in strain sensitivity to drug toxicity and drug effectiveness in different tumor-host systems was observed. Increased median survival time with reversal of tumor-induced immune dysfunction, without toxicity to hematopoietic progenitor cells, was realized in two tumor-host-drug combinations. Polyinosinic-polycytidylic acid was effective against J774, while actinomycin D was active against 70Z/2. Mitomycin C effectively reduced tumor load, as evidenced by loss of splenic tumor colony-forming cells for all three tumors. This agent prolonged survival and concomitantly restored immunological responsiveness in hosts immunosuppressed by growth of 70Z/2 or J774. Paralleling tumor reduction with mitomycin C therapy, the splenic hematopoietic progenitor and colony-forming B-cells were reduced in tumor-bearing and tumor-free mice, thus compromising its therapeutic effectiveness. 1-beta-D-Arabinofuranosylcytosine reduced tumor load with marginal toxicity toward hematopoietic progenitor and colony-forming B-cells. However, immune responsiveness was only partially restored, and median survival was not increased. The results presented show the diversity of therapeutic drug effectiveness in increasing mean survival time and influencing other life-sustaining parameters (immunological and hematopoietic functions).

Animals↗
PubMed1979

Correlation of extracts obtained by high efficiency gel chromatography of lactic dehydrogenase virus infected mouse serum and cytosol from human tumors using leukocyte adherence inhibition assay.

Immunochemically active fractions were obtained using Separon Hema-300-glc(R) from serum of lactic dehydrogenase virus (LDV) infected mice and from homogenates of human tumors. The mixture of proteins of tumorous origin from the cytosol giving a positive reaction in the leukocyte adherence inhibition (LAI) test was found in the same fractions showing maximum of absorbance at 340 nm in the spectrophotometer and a corresponding peak in the refractometer. Analogous peaks were not proved in material obtained from healthy controls, but they were found in some human placentas and fetal organs. The LDV fraction obtained from mouse serum served as a "control" antigen in LAI test for human tumor testing, and results corresponded with those obtained using cytosol specific for the tumor under study.

Animals↗
PubMed1977

Immunodepression, ascites tumour and lactate dehydrogenase virus.

The delayed hypersensitivity (DH) response to picryl chloride was studied in Ehrlich ascites tumour-bearing and normal control mice. A significant depression of the DH response was found in the tumour-bearing mice, which was associated with a marked elevation of serum lactate dehydrogenase (LDH). Depression of DH was also observed in mice receiving cell-free ascitic fluid. These mice also showed an elevated serum LDH which is assumed to be associated with the lactate dehydrogenase virus. A method for assaying DH in vivo is described.

Animals↗