Dog Kidney Cells Research Articles

Adriamycin stimulates canine kidney (mdck) cells to deacylate cellular lipids and to produce prostaglandins.

Dog kidney (MDCK) cells treated with adriamycin (0.5 μg/ml) for 1 hr, produced from 2 to 7 times more prostaglandins E 2 and F 2α when measured in culture media 24, 48 and 72 hrs after the treatment. Indomethacin (ID 50 <2 × 10 −8 M) and cycloheximide (0.5 μg/ml) inhibited this adriamycin-stimulated prostaglandin production. The aglycone of adriamycin (0.5 to 5.0 μg/ml) had little stimulating effect. Treatment of [ 3H]arachidonic acid-labeled MDCK cells with adriamycin (0.5 μg/ml) for 1 hr also stimulated deacylation of cellular lipids during subsequent incubation. Altered morphology of MDCK cells resulted from such treatment with adriamycin; indomethacin did not inhibit this change, but cycloheximide did.

Reversion to Virulence of Attenuated Canine Distemper Virus In Vivo and In Vitro

SUMMARY Reversion to virulence of dog kidney cell attenuated canine distemper virus (CDV), Rockborn strain, was demonstrated after serial passage in dogs. The same strain also reverted to virulence after serial passage in canine macrophage cultures. Criteria for virulence in dogs included clinical signs, weight loss, elevated body temperatures, reduced total lymphocyte counts, impaired blastogenesis responses of blood lymphocytes, appearance of virus antigen in epithelial cells, the character of neutralizing antibody responses and the capability of re-isolated virus to grow in canine macrophage cultures.

Isolation of amiloride-resistant clones from dog kidney epithelial cells.

The diuretic drug amiloride has been used to select variants from the dog kidney cell line MDCK which are partially resistant to killing by the drug. Evidence is presented suggesting that resistance to killing by amiloride is conferred by decreased uptake of amiloride, which reduces the intracellular drug concentration below the toxic level.

Small-plaque variant of canine herpesvirus with reduced pathogenicity for newborn pups

The plaque characteristics of 13 field isolates of canine herpesvirus were found to be similar. After 312 passages of the F-205 strain in dog kidney cell cultures incubated at 35 degrees C, the virus still was virulent for newborn pups; it also had the macroplaque morphology of the wild-type virus. However, after 20 additional passages at 30 degrees C, a microplaque (mP) variant had emerged as the predominant type. Cloned mP virus retained the small-plaque characteristic after 66 transfers at 30 degrees C. The natural history of the mP strain and some of its biological properties are reported, the most significant being its lack of pathogenicity for newborn pups.

Production of group- and type-specific antigens during non-permissive infection of dog kidney cells with herpes simplex virus type 2

Infection of a continuous cell line of dog kidney origin (MDCK) with herpes simplex virus type 2 (HSV-2) resulted in production of little to no new infectious virus. Serial subculture of MDCK cells inoculated with HSV-2 did not permit establishment of carrier cell cultures, as assessed by negative results of plaque assays for infectious virus and radioimmunoassay (RIA) for viral antigens. Group- and type-specific antigens were detected in lysates of non-permissive MDCK cells inoculated with HSV-2 and tested by RIA at 24 hours post-inoculation. Polypeptides produced in permissive (Vero) and non-permissive (MDCK) cell systems were labeled with [ 14C]-amino acids and analyzed by polyacrylamide slab gel electrophoresis and autoradiography. During non-permissive infection, two polypeptides of large molecular weight, not found in uninfected MDCK cells, one of which commigrated with a major HSV-2 structural polypeptide, were synthesized and reproducibly detected.

Effects of phorbol-12,13-diesters on prostaglandin production and phospholipase activity in canine kidney (MDCK) cells

Two tumor promoting phorbol-12,13-diesters, 12-0-tetradecanoyl-phorbol-13-acetate and phorbol-12,13-didecanoate, at concentrations of 10 −9 to 10 −10 M, stimulated prostaglandin production by dog kidney (MDCK) cells cultured in serum-supplemented medium. The non-tumor producing phorbol diester, 4α-phorbol-12,13-didecanoate, at a concentration of 10 −7 M, had no effect. The two biologically active phorbol diesters, but not the non-tumor promoting analog, stimulated deacylation of the cellular phospholipids of MDCK cells radioactively labelled with [ 3H]arachidonic acid. Most of the arachidonic acid was converted into prostaglandins.

Antibody stimulation of tumor cells.

Antiserum to normal dog kidney cells was found to stimulate cell division in a transformed dog kidney cell line. The stimulation is obtained with the γ-globulin fraction of the antiserum and the effect is removed by absorption of the antiserum with either the transformed dog kidney cell or with primary dog kidney cells. No adaptation to the antiserum occurred after seven passages in antiserum; the cells were still stimulated by the antiserum as compared to normal serum. Because antibody to normal tissues occurs following injury, it is proposed that this may explain the promotion of tumors by tissue injury.

Epidermal growth factor stimulates prostaglandin biosynthesis by canine kidney (MDCK) cells

Serum and/or arachidonic acid stimulated prostaglandin production by dog kidney (MDCK) cells. Epidermal growth factor (EGF) at concentrations of 10 −9 to 10 −10 M stimulated the biosynthesis of prostaglandins by MDCK cells but not that by human fibroblasts (D-550), mouse fibroblasts (3T3), transformed mouse fibroblasts (MC5-5), and rabbit aorta endothelial cells (CLO). EGF also stimulated the release of radioactivity from MDCK cells radioactively labelled with [ 3H]arachidonic acid.

Effect of Canine Adenovirus on JINET and Vero Cells

Two simian cell lines, JINET and vero, were inoculated with infectiouscanine hepatitis virus at a variety of input multiplicity. The viral effects observed onthem were compared with those on primary dog kidney cells. Infected cell cultures andrecovered viruses were subjected to serial passages.In JINET cells, virus titer remained constant without showing an increase. None ofinclusion body and hemagglutinating and complement-fixing antigens were detected.Cytopathic effect occurred only when virus of high input multiplicity was inoculated.Immunofluorescent viral antigen was visible in a small number of cells. In vero cells, specifically fluorescent cells and infective viruses appeared at lower levels than in JINETcells, and no other changes associated with the virus infection were detected. Comparisonof surface morphology was made by scanning electron microscopy among the three kindsof cell cultures. It revealed that patterns for every degree of cytopathic changes corre-sponded to those described above.

Plaque Formation with Influenza Viruses in Dog Kidney Cells

Infectious influenza and parainfluenza viruses were produced as plaql passages of egg-grown viruses in MDCK monolayers. Virus titres of 10(6) to 10(11) p.f.u./ml were obtained for several A and B strains of influenza and parainfluenza viruses.

Acetylation and Phosphorylation of Chromosomal Proteins in Dog Kidney Cells Infected with Infectious Canine Hepatitis Virus

Acetylation and Phosphorylation of Chromosomal Proteins in Dog Kidney Cells Infected with Infectious Canine Hepatitis Virus

HEPATITIS IN SKUNKS CAUSED BY THE VIRUS OF INFECTIOUS CANINE HEPATITIS

Two cases of acute, fatal, hepatitis occurred in young, striped skunks (Mephitis mephitis) trapped in southern Ontario. Histologically, lesions in the liver were similar to infectious canine hepatitis. A virus was isolated which produced large intranuclear inclusions in dog kidney cell cultures. These inclusions were Feulgen-positive and fluoresced green with acridine orange stain. The skunk hepatitis isolate was identified as the virus of infectious canine hepatitis by virus neutralization tests.

Phosphorylation of nonhistone chromosomal proteins in dog kidney cells infected with infectious canine hepatitis virus

Infectious canine hepatitis virus infection of dog kidney cells altered the metabolism of the nonhistone chromosomal proteins. The rate of incorporation of [ 32P]phosphate into the nonhistone chromosomal proteins began to increase between 6 and 7 hr after infection, and the specific activity of the proteins labeled between 8 and 9 hr after infection was 195% of that observed in the mock-infected control. Analysis by sodium dodecyl sulfate polyacrylamide gel electrophoresis showed that phosphorylation of the nonhistone chromosomal proteins was increased after infection especially in some particular components of the proteins. Alteration of the metabolism of the nonhistone chromosomal proteins correlated with an increase of RNA synthesis and template activity of chromatin in infected cells.

Persistence of measles antibody after immunization

The authors followed up the persistence of measles antibodies at 1-year intervals in children given three different live attenuated measles vaccines. The best results were obtained in a group of children given the attenuated Schwarz strain vaccine; this vaccine, prepared in chick embryo cells, consistently produced sero-conversion rates of 92% over a period of 2–6 years. The lowest sero-conversion rate was observed in children given the Edmonston strain vaccine prepared on dog-kidney cells; here, the vaccine induced a sero-conversion rate of 66% after 5–6 years following the immunization. Proportions of seronegative children in three groups of children, administered the Schwarz strain vaccine, prepared on dog-kidney cells, were shown to vary; nevertheless, no statistically significant differences among these groups could be demonstrated. The average sero-conversion rates in the three groups of children were 97, 91, 85 and 82% following 1, 2, 3 and 4 years after immunization, respectively. The greatest decline in antibody titre was shown to occur between 1 month and 1 year after vaccination. In subsequent years these values may vary.

Studies on Reovirus Infection in Canine Cells by the Fluorescent Antibody Technique

Changes induced in primary dog kidney cell cultures by reovirus infection were investigated sequentially by virus and antigen estimations, conventional staining and direct fluorescent antibody techniques. Specific fluorescence was first detected 8-10 hours after infection and extended finally all over the cytoplasm. Fluorescence and cytoplasmic inclusion bodies were found to appear in five sequential stages distinguished by shape and location in the cell. These stages were in parallel to virus infectivity and hemagglutinating and complement-fixing antigenicity. Cytoplasmic immunofluorescence was also detectable in the throat smear of pups experimentally exposed to reovirus aerosols. The fluorescent antibody technique seemed to be a useful means for the rapid diagnosis of reovirus infection when applied to field cases.

Immune Electron Microscopy (IEM) of a Canine Adeno-Associated Virus

In 1968, Sugimura and Yanagawa described a small 25 nm virus like particle in association with the Matsuda strain of infectious canine hepatitis virus (ICHV). Domoto and Yanagawa showed that this particle was dependent on ICHV for its replication in primary dog kidney cell cultures (PDK) and was resistant to heating at 70°C for 10 min, and concluded that it was a canine adeno-associated virus (CAAV). Later studies by Onuma and Yanagawa compared CAAV with the known human serotypes (AAV 1, 2, 3) and AAV-4, known to be associated with African Green Monkeys. Using the complement fixation (CF) test, they found that CAAV was serologically related to AAV-3 and had wide distribution in the dog population of Japan.

Polyneuropathy following rubella immunization. A follow-up study and review of the problem.

Thirty-two children with post-rubella-immunization neuropathies were observed for up to 32 months. Twenty children (62%) had no subsequent symptoms. Ten (31%) had minor complaints that included features of their initial complications. Only two children (6%) had major recurrences. These episodes occurred periodically throughout the 2½-year follow-up period. Both recurrences were of the leg syndrome (catcher's crouch). Review of the literature indicates that neuropathy is an occasional complication of both natural rubella and immunization with live, attenuated rubella virus vaccines, especially the one prepared in dog kidney cells. The dog kidney cell vaccine is no longer in use. Currently available vaccines remain acceptable for continued use in public and private programs.

Origin of thymidine kinase in the cells infected with infectious canine hepatitis virus.

ABSTRACTThymidine kinase (TK) was induced in dog kidney cells (DKC) and hamster embryo cells (HEC) infected with infectious canine hepatitis virus (ICHV). The enzyme activity increased and reached levels of 13 and 19 times as much as in uninfected cells by the 30th hr after infection in virus‐infected DKC and HEC, respectively. No difference in the pattern of inactivation at 45 C was found between the TK of infected and uninfected cells. The activity of the TK from ICHV‐infected DKC was not inhibited by a dog serum hyperimmunized against ICHV‐infected DKC. From these results it was concluded that the TK which increased in ICHV‐infected cells was of the cellular origin.

Electron microscope study of the morphogenesis of a new canine herpesvirus in dog kidney cells.

The ultrastructural morphogenesis of the CHV-BR strain canine herpesvirus (CHV) grown in dog kidney cells is described. The sequence of virus development differs from that described previously for other CHV strains grown in dog kidney cells and resembles closely that of herpes simplex virus and several animal herpesviruses.

Electron microscopic study of nuclear and nucleolar changes in cells infected with canine distemper virus (CDV)

The nuclear changes occurring in dog kidney cells infected with a virulent and an attenuated strain of canine distemper virus were examined by electron microscopy. No ultrastructural evidence for intranuclear virus replication was observed even though large eosinophilic nuclear inclusions were found in up to 34% of infected cells examined by light microscopy. This discrepancy between light and electron microscopic findings was discussed in relation to the possible structure of the nuclear inclusions. Marked morphological changes were noted in the nucleoli of up to 12% of cells infected with the virulent strain, CDV/BR, involving complete segregation of the granular and fibrillar components. The nucleolar lesions were similar to those induced by chemical inhibitors of cellular nucleic acid metabolism.