Effect of interleukin-18 on viral myocarditis: enhancement of interferon- gamma and natural killer cell activity. 2000

T Kanda, and T Tanaka, and K Sekiguchi, and Y Seta, and M Kurimoto, and J E Wilson McManus, and R Nagai, and D Yang, and B M McManus, and I Kobayashi
Department of General Medicine, Gunma University School of Medicine, 3-39-15, Showa-machi, Maebashi, 371, Japan. kanda@sb.hunma-u.ac.jp

Encephalomyocarditis virus causes viral myocarditis with myocyte necrosis and inflammatory cell infiltration in mice. Because previous studies have shown that some cytokines prevent the sequelae of myocarditis, we assessed the effect of a newly identified cytokine, interleukin-18 (IL-18), in preventing the sequelae of myocarditis. Murine IL-18 (10 microg/day/mouse) was given peritoneally for 10 days in C3H mice infected with EMC virus. Mice were divided into group IL-18 (infected-treated), saline group (infected-untreated), group IL-18-2 (treatment started on day 2), group IL-18-5 (treatment started on day 5). Although the 14-day survival rate in saline group was 20%, that in the group IL-18 increased to 80% (P<0.05). Either mice in group IL-18-2 or in group IL-18-5 did not survive longer than saline group. The viral titer of the heart on day 3 was lower in group IL-18 compared to the saline group (1.00+/-0.20 log(10)tissue culture infected dose (TCID)(50)/mg wet weight v 1.42+/-0.12 log(10)TCID(50)/mg, n=3 of each). Mice in group IL-18 had less myocardial necrosis and cellular infiltration than the saline group. The myocardial expression of interferon- gamma (IFN- gamma) mRNA in group IL-18 was significantly (P<0.05) greater than the saline group on days 1 and 3 after viral inoculation. Circulating IFN- gamma was significantly elevated on days 1, 5, and 7, but significantly reduced on day 3. The natural killer cell activities in the spleen on days 1, 3, and 5 were significantly (P<0.05) greater in group IL-18 than in the saline group (41+/-9%v 10+/-6% on day 3, 4 of each). We conclude that IL-18 reduces the severity of EMC viral myocarditis by inducing cardiac expression of IFN- gamma mRNA and increasing splenic natural killer cell activity.

UI MeSH Term Description Entries
D007371 Interferon-gamma The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES. Interferon Type II,Interferon, Immune,gamma-Interferon,Interferon, gamma,Type II Interferon,Immune Interferon,Interferon, Type II
D007694 Killer Cells, Natural Bone marrow-derived lymphocytes that possess cytotoxic properties, classically directed against transformed and virus-infected cells. Unlike T CELLS; and B CELLS; NK CELLS are not antigen specific. The cytotoxicity of natural killer cells is determined by the collective signaling of an array of inhibitory and stimulatory CELL SURFACE RECEPTORS. A subset of T-LYMPHOCYTES referred to as NATURAL KILLER T CELLS shares some of the properties of this cell type. NK Cells,Natural Killer Cells,Cell, NK,Cell, Natural Killer,Cells, NK,Cells, Natural Killer,Killer Cell, Natural,NK Cell,Natural Killer Cell
D008809 Mice, Inbred C3H An inbred strain of mouse that is used as a general purpose strain in a wide variety of RESEARCH areas including CANCER; INFECTIOUS DISEASES; sensorineural, and cardiovascular biology research. Mice, C3H,Mouse, C3H,Mouse, Inbred C3H,C3H Mice,C3H Mice, Inbred,C3H Mouse,C3H Mouse, Inbred,Inbred C3H Mice,Inbred C3H Mouse
D009205 Myocarditis Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies. Carditis,Myocarditides
D009336 Necrosis The death of cells in an organ or tissue due to disease, injury or failure of the blood supply.
D009929 Organ Size The measurement of an organ in volume, mass, or heaviness. Organ Volume,Organ Weight,Size, Organ,Weight, Organ
D004686 Encephalomyocarditis virus The type species of CARDIOVIRUS causing encephalomyelitis and myocarditis in rodents, pigs, and monkeys. Infection in man has been reported with CNS involvement but without myocarditis. EMCV
D005260 Female Females
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D012333 RNA, Messenger RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm. Messenger RNA,Messenger RNA, Polyadenylated,Poly(A) Tail,Poly(A)+ RNA,Poly(A)+ mRNA,RNA, Messenger, Polyadenylated,RNA, Polyadenylated,mRNA,mRNA, Non-Polyadenylated,mRNA, Polyadenylated,Non-Polyadenylated mRNA,Poly(A) RNA,Polyadenylated mRNA,Non Polyadenylated mRNA,Polyadenylated Messenger RNA,Polyadenylated RNA,RNA, Polyadenylated Messenger,mRNA, Non Polyadenylated

Related Publications

T Kanda, and T Tanaka, and K Sekiguchi, and Y Seta, and M Kurimoto, and J E Wilson McManus, and R Nagai, and D Yang, and B M McManus, and I Kobayashi
December 1988, Zhonghua xin xue guan bing za zhi,
T Kanda, and T Tanaka, and K Sekiguchi, and Y Seta, and M Kurimoto, and J E Wilson McManus, and R Nagai, and D Yang, and B M McManus, and I Kobayashi
April 1990, Chinese medical journal,
T Kanda, and T Tanaka, and K Sekiguchi, and Y Seta, and M Kurimoto, and J E Wilson McManus, and R Nagai, and D Yang, and B M McManus, and I Kobayashi
September 1983, Infection and immunity,
T Kanda, and T Tanaka, and K Sekiguchi, and Y Seta, and M Kurimoto, and J E Wilson McManus, and R Nagai, and D Yang, and B M McManus, and I Kobayashi
March 1983, Biochemical and biophysical research communications,
T Kanda, and T Tanaka, and K Sekiguchi, and Y Seta, and M Kurimoto, and J E Wilson McManus, and R Nagai, and D Yang, and B M McManus, and I Kobayashi
March 2004, Immunology,
T Kanda, and T Tanaka, and K Sekiguchi, and Y Seta, and M Kurimoto, and J E Wilson McManus, and R Nagai, and D Yang, and B M McManus, and I Kobayashi
September 2003, Journal of virology,
T Kanda, and T Tanaka, and K Sekiguchi, and Y Seta, and M Kurimoto, and J E Wilson McManus, and R Nagai, and D Yang, and B M McManus, and I Kobayashi
April 1979, Cellular immunology,
T Kanda, and T Tanaka, and K Sekiguchi, and Y Seta, and M Kurimoto, and J E Wilson McManus, and R Nagai, and D Yang, and B M McManus, and I Kobayashi
August 1987, Gastroenterologia Japonica,
T Kanda, and T Tanaka, and K Sekiguchi, and Y Seta, and M Kurimoto, and J E Wilson McManus, and R Nagai, and D Yang, and B M McManus, and I Kobayashi
December 1987, Scandinavian journal of immunology,
T Kanda, and T Tanaka, and K Sekiguchi, and Y Seta, and M Kurimoto, and J E Wilson McManus, and R Nagai, and D Yang, and B M McManus, and I Kobayashi
January 1980, Annales d'immunologie,
Copied contents to your clipboard!