Open Access. Powered by Scholars. Published by Universities.®

Medicine and Health Sciences Commons

Open Access. Powered by Scholars. Published by Universities.®

Articles 1 - 9 of 9

Full-Text Articles in Medicine and Health Sciences

Cellular Basis Of Decreased Immune Responses To Pneumococcal Vaccines In Aged Mice, Manju Garg, Wei Luo, Alan M. Kaplan, Subbarao Bondada Nov 1996

Cellular Basis Of Decreased Immune Responses To Pneumococcal Vaccines In Aged Mice, Manju Garg, Wei Luo, Alan M. Kaplan, Subbarao Bondada

Microbiology, Immunology, and Molecular Genetics Faculty Publications

Previously, model systems were developed in our laboratory to study murine immune responses to the 23-valent pneumococcal polysaccharide vaccine Pnu-Imune, both in vivo and in vitro (M. Garg and B. Subbarao, Infect. Immun. 60:2329-2336, 1992; M. Garg, A. M. Kaplan, and S. Bondada, J. Immunol. 152: 1589-1596, 1994). Using these systems, we found that aged mice did not respond to the vaccine in vivo or in vitro. Cell separation studies showed that the unresponsiveness of the aged spleen cells to the vaccine was not due to an intrinsic B-cell defect or to T-cell-mediated immunosuppression but resulted from an accessory cell …


Attachment Of Toxoplasma Gondii To Host Cells Is Host Cell Cycle Dependent., Jane Grimwood, Jose R. Mineo, Lloyd H. Kasper Oct 1996

Attachment Of Toxoplasma Gondii To Host Cells Is Host Cell Cycle Dependent., Jane Grimwood, Jose R. Mineo, Lloyd H. Kasper

Dartmouth Scholarship

The initial attachment of Toxoplasma tachyzoites to target host cells is an important event in the life cycle of the parasite and hence critical in the pathogenesis of this infection. The efficiency of Toxoplasma attachment to synchronized populations of Chinese hamster ovary cells and bovine kidney cells was investigated by using a glutaraldehyde-fixed host cell assay system. For both cell lines, parasite attachment increased as the synchronized host cells proceeded from the G1 phase to the mid-S phase and then decreased as the cells entered the G2-M boundary. Postulating that these differences in attachment reflect the upregulation of a specific …


Activation Of The Human Thymidine Kinase (Tk) Promoter By Simian Virus 40 Large T Antigen Requires Both The T Antigen Prb Family-Binding Domain And Tk Promoter Sequences Resembling E2f-Binding Sites., Michelle M. Anderson, Jun Chen, Charles N. Cole, Susan E. Conrad Sep 1996

Activation Of The Human Thymidine Kinase (Tk) Promoter By Simian Virus 40 Large T Antigen Requires Both The T Antigen Prb Family-Binding Domain And Tk Promoter Sequences Resembling E2f-Binding Sites., Michelle M. Anderson, Jun Chen, Charles N. Cole, Susan E. Conrad

Dartmouth Scholarship

Infection of quiescent cells with the DNA tumor virus simian virus 40 induces expression of the cellular thymidine kinase (TK) gene a minimum of 10- to 20-fold, and this induction depends upon the viral protein large T antigen (T-Ag). To define both human TK promoter elements and T-Ag functional domains required for transcriptional induction, we have established a system in which stable Rat-1 transfectants harboring TK promoter-luciferase hybrid genes are infected with recombinant adenoviruses expressing either wild-type or mutant forms of T-Ag and luciferase expression is measured as an indicator of promoter activity. The results show that (i) a 135-bp …


Differential Expression Of The Toxr Regulon In Classical And E1 Tor Biotypes Of Vibrio Cholerae Is Due To Biotype-Specific Control Over Toxt Expression., Victor J. Dirita, Melody Neely, Ronald K. Taylor, Paul M. Bruss Jul 1996

Differential Expression Of The Toxr Regulon In Classical And E1 Tor Biotypes Of Vibrio Cholerae Is Due To Biotype-Specific Control Over Toxt Expression., Victor J. Dirita, Melody Neely, Ronald K. Taylor, Paul M. Bruss

Dartmouth Scholarship

The two major disease-causing biotypes of Vibrio cholerae, classical and El Tor, exhibit differences in their epidemic nature. Their behavior in the laboratory also differs in that El Tor strains produce two major virulence factors, cholera toxin (CT) and the toxin coregulated pilus (TCP), only under very restricted growth conditions, whereas classical strains do so in standard laboratory medium. Expression of toxin and TCP is controlled by two activator proteins, ToxR and ToxT, that operate in cascade fashion with ToxR controlling the synthesis of ToxT. Both biotypes express equivalent levels of ToxR, but only classical strains appear to express ToxT …


Toxin-Coregulated Pilus, But Not Mannose-Sensitive Hemagglutinin, Is Required For Colonization By Vibrio Cholerae O1 El Tor Biotype And O139 Strains., K Helene Thelin, Ronald K. Taylor Jul 1996

Toxin-Coregulated Pilus, But Not Mannose-Sensitive Hemagglutinin, Is Required For Colonization By Vibrio Cholerae O1 El Tor Biotype And O139 Strains., K Helene Thelin, Ronald K. Taylor

Dartmouth Scholarship

The relative contributions of toxin-coregulated pilus (TCP) and cell-associated mannose-sensitive hemagglutinin (MSHA) to the colonization ability of Vibrio cholerae O1 El Tor biotype strains and O139 Bengal strains was determined by using isogenic parental and in-frame deletion mutant pairs in the infant mouse cholera model. Both the El Tor and O139 tcpA mutant strains showed a dramatic defect in colonization as indicated by their competitive indices, whereas deletion of mshA had a negligible effect on colonization in either background.


Toxoplasma Gondii-Induced Immune Suppression By Human Peripheral Blood Monocytes: Role Of Gamma Interferon., Jacqueline Y. Channon, Lloyd H. Kasper Apr 1996

Toxoplasma Gondii-Induced Immune Suppression By Human Peripheral Blood Monocytes: Role Of Gamma Interferon., Jacqueline Y. Channon, Lloyd H. Kasper

Dartmouth Scholarship

The ability of Toxoplasma gondii to evade the host immune response during primary infection in humans is poorly understood. In murine toxoplasmosis, infected spleen macrophages release soluble factors that mediate a transient immunosuppression, which may allow the parasite to become established. When an enriched population of human monocytes from seronegative individuals was incubated with toxoplasmas in vitro, soluble factors that mediated market suppression of mitogen-induced lymphocyte DNA synthesis were released. Irradiated tachyzoites that do not undergo replication were sufficient stimuli for near-maximal soluble factor release. Up to 50% of the soluble factor-mediated suppression is attributable to a gamma interferon (IFN-gamma)-dependent …


Antibody To The Ligand For Cd40 (Gp39) Inhibits Murine Aids-Associated Splenomegaly, Hypergammaglobulinemia, And Immunodeficiency In Disease-Susceptible C57bl/6 Mice., Kathy A. Green, Karen M. Crassi, Jon D. Laman, Arjan Schoneveld, Rendall R. Strawbridge, Teresa M. Foy, Randolph J. Noelle, William R. Green Apr 1996

Antibody To The Ligand For Cd40 (Gp39) Inhibits Murine Aids-Associated Splenomegaly, Hypergammaglobulinemia, And Immunodeficiency In Disease-Susceptible C57bl/6 Mice., Kathy A. Green, Karen M. Crassi, Jon D. Laman, Arjan Schoneveld, Rendall R. Strawbridge, Teresa M. Foy, Randolph J. Noelle, William R. Green

Dartmouth Scholarship

Infection of genetically susceptible C57BL/6 mice with the LP-BM5 isolate of murine retroviruses cause profound splenomegaly, hypergammaglobulinemia, lymphadenopathy, and an immunodeficiency syndrome which includes the development of terminal B-cell lymphomas. Because many of these and the other manifestations of LP-BM5 virus-induced disease are similar to those seen in AIDS, this syndrome has been named murine AIDS, or MAIDS. Previous reports have shown that the onset of MAIDS depends on the presence of both CD41 T cells and B cells and have suggested that CD41 T-cell-B-cell interactions are important to disease pathogenesis. Here, we assessed the possibility that interactions between CD40 …


A Tandem Duplication Within The Fibrillin 1 Gene Is Associated With The Mouse Tight Skin Mutation., Linda D. Siracusa, Rodney Mcgrath, Qing Ma, John J. Moskow, Jayanthi Manne, Paul J. Christner, Arthur M. Buchberg, Sergio A. Jimenez Apr 1996

A Tandem Duplication Within The Fibrillin 1 Gene Is Associated With The Mouse Tight Skin Mutation., Linda D. Siracusa, Rodney Mcgrath, Qing Ma, John J. Moskow, Jayanthi Manne, Paul J. Christner, Arthur M. Buchberg, Sergio A. Jimenez

Department of Medicine Faculty Papers

Mice carrying the Tight skin (Tsk) mutation have thickened skin and visceral fibrosis resulting from an accumulation of extracellular matrix molecules. These and other connective tissue abnormalities have made Tskl + mice models for scleroderma, hereditary emphysema, and myocardial hypertrophy. Previously we localized Tsk to mouse chromosome 2 in a region syntenic with human chromosome 15. The microfibrillar glycoprotein gene, fibrillin 1 (FBN1), on human chromosome 15q, provided a candidate for the Tsk mutation. We now demonstrate that the Tsk chromosome harbors a 30- to 40-kb genomic duplication within the Fbn1 gene that results in a larger than normal in-frame …


Analysis Of The Effects Of Overexpression Of Metallothionein-I In Transgenic Mice On The Reproductive Toxicology Of Cadmium., T Dalton, Kai Fu, G C Enders, R D Palmiter, G K Andrews Jan 1996

Analysis Of The Effects Of Overexpression Of Metallothionein-I In Transgenic Mice On The Reproductive Toxicology Of Cadmium., T Dalton, Kai Fu, G C Enders, R D Palmiter, G K Andrews

Journal Articles: Pathology and Microbiology

Exposure to low levels of cadmium reduces fertility. In male mice spermatogenesis is highly sensitive to cadmium, whereas in females the peri-implantation period of pregnancy is sensitive. To examine the potential roles of the cadmium-binding protein, metallothionein (MT), in the reproductive toxicology of cadmium, we examined a transgenic mouse strain that overexpresses metallothionein-I (MT-I). These mice had dramatically increased steady-state levels of MT-I mRNA and MT in the testes and in the female reproductive tract during the peri-implantation period of pregnancy, and this overexpression occurred in a cell-specific and temporally regulated manner similar to that of the endogenous MT-I gene. …