+publisher:"Texas A&M University" +contributor:("Tesh, Vernon")

Texas A&M University

1. Weber, Mary. Identification of C. burnetii Type IV Secretion Substrates Required for Intracellular Replication and Coxiella-Containing Vacuole Formation.

Degree: PhD, Medical Sciences, 2014, Texas A&M University

URL: http://hdl.handle.net/1969.1/152608

► Coxiella burnetii is a Gram-negative intracellular pathogen that encodes a specialized type IVb secretion system (T4SS) which is essential for intracellular replication, Coxiella-containing vacuole (CCV)… (more)

Subjects/Keywords: Coxiella; T4SS; Effector

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APA (6^th Edition):

Weber, M. (2014). Identification of C. burnetii Type IV Secretion Substrates Required for Intracellular Replication and Coxiella-Containing Vacuole Formation. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/152608

Chicago Manual of Style (16^th Edition):

Weber, Mary. “Identification of C. burnetii Type IV Secretion Substrates Required for Intracellular Replication and Coxiella-Containing Vacuole Formation.” 2014. Doctoral Dissertation, Texas A&M University. Accessed February 28, 2021. http://hdl.handle.net/1969.1/152608.

MLA Handbook (7^th Edition):

Weber, Mary. “Identification of C. burnetii Type IV Secretion Substrates Required for Intracellular Replication and Coxiella-Containing Vacuole Formation.” 2014. Web. 28 Feb 2021.

Vancouver:

Weber M. Identification of C. burnetii Type IV Secretion Substrates Required for Intracellular Replication and Coxiella-Containing Vacuole Formation. [Internet] [Doctoral dissertation]. Texas A&M University; 2014. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1969.1/152608.

Council of Science Editors:

Weber M. Identification of C. burnetii Type IV Secretion Substrates Required for Intracellular Replication and Coxiella-Containing Vacuole Formation. [Doctoral Dissertation]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/152608

Texas A&M University

2. McGruder, Brenna Mariechen. Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease.

Degree: PhD, Medical Sciences, 2014, Texas A&M University

URL: http://hdl.handle.net/1969.1/152630

► A targeted recombination system was developed for MHV-1 by generation of a Donor plasmid that consisted of sequences consisting of the first 448 nucleotides of… (more)

▼ A targeted recombination system was developed for MHV-1 by generation of a Donor plasmid that consisted of sequences consisting of the first 448 nucleotides of the MHV-1 genome fused to sequences from codon 28 in the HE gene through the 3’UTR to the poly(A) tail. The Donor plasmid was transcribed in vitro and transfected into FCWF cells that had been infected with a felinized MHV-1 recombinant virus. Recombinant viruses were selected by overlaying infected/transfected FCWF cells onto murine DBT cells and monitoring for syncytia formation and cell death. Recombinant viruses were plaque purified and expanded in murine cells. Several recombinant viruses that were not significantly different from MHV-1 in tissue culture were isolated, but none were pneumopathogenic in the A/J mouse. During the generation of multiple wild type MHV-1 stocks for mouse studies we discovered that MHV-1 rapidly lost pnuemopathogenicity during passage in DBT cells. This finding demonstrated that targeted recombination may not be a viable method of genetic manipulation of MHV-1 because the multiple passages in cell culture required to generate viruses by targeted recombination may cause loss of virulence. Using Next-Generation sequencing technology a virulent and non-virulent MHV-1 passage were sequenced, and two potential mutations that are present in the subpopulation of virulent viruses were identified that may contribute to pneumopathogenicity: nsp13 C17015A and ns4 G28454A. We are developing an infectious cDNA clone using in vitro assembly of MHV-1 cDNA fragments. The fragments are flanked by type II restriction enzymes which, when digested liberate cDNA fragments that only contain MHV-1 genetic sequence and can be ligated together. By housing portions of the MHV-1 genome in low-copy plasmids we were able to create a system that is easily maintained in bacteria and easily manipulated by restriction digestion or site-directed mutagenesis. This infectious clone will be used to determine if the mutations that were discovered during the sequencing of the MHV-1 pneumovirulent virus are sufficient and able to generate a pnueumopathogenic virus. The infectious clone will also be used to determine the role, if any, of ns2 in an MHV-1 infection of lungs. Advisors/Committee Members: Leibowitz, Julian (advisor), Payne, Susan (committee member), Tesh, Vernon (committee member), Welsh, Jane (committee member).

Subjects/Keywords: MHV-1; lung pathogenesis, SARS-CoV; mouse hepatitis virus strain 1; reverse genetic; whole genome

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APA (6^th Edition):

McGruder, B. M. (2014). Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/152630

Chicago Manual of Style (16^th Edition):

McGruder, Brenna Mariechen. “Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease.” 2014. Doctoral Dissertation, Texas A&M University. Accessed February 28, 2021. http://hdl.handle.net/1969.1/152630.

MLA Handbook (7^th Edition):

McGruder, Brenna Mariechen. “Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease.” 2014. Web. 28 Feb 2021.

Vancouver:

McGruder BM. Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease. [Internet] [Doctoral dissertation]. Texas A&M University; 2014. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1969.1/152630.

Council of Science Editors:

McGruder BM. Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease. [Doctoral Dissertation]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/152630

Texas A&M University

3. Harrison, Lisa Margaret. The effects of Shiga toxin 1 on cytokine and chemokine production and apoptosis in a human monocytic cell line.

Degree: PhD, Medical Sciences, 2004, Texas A&M University

URL: http://hdl.handle.net/1969.1/1038

► Severe bloody diarrhea and subsequent serious post-diarrheal illnesses, including the hemolytic uremic syndrome and central nervous system complications, may develop following infections with Shiga toxin… (more)

▼ Severe bloody diarrhea and subsequent serious post-diarrheal illnesses, including the hemolytic uremic syndrome and central nervous system complications, may develop following infections with Shiga toxin (Stx)-producing bacteria. The cytotoxic actions of Stxs destroy the microvasculature of organs, preventing function. A role for the cytokines tumor necrosis factor-alpha (TNF-[alpha]) and interleukin-1 beta (IL-1[beta]) in exacerbating disease may lie in their ability to up-regulate the Stx receptor, Gb3, on endothelial cell surfaces. A main source of proinflammatory cytokines is the macrophage, thus leading us to utilize the monocytic/macrophage-like cell line, THP-1, as a model for cytokine production in Stx pathogenesis. In addition to treating THP-1 cells with purified Stx1, cells were also treated with lipopolysaccharides (LPS), since bacterial LPS are known to be potent inducers of cytokines, and may be present during infection. Undifferentiated THP-1 cells are sensitive to Stx1 and do not produce TNF-[alpha] or IL-1[beta], while differentiated THP-1 cells, a better model for resident tissue macrophages, are less sensitive to Stx1 and produce TNF-[alpha] and IL-1[beta]. Prolonged expression of TNF-[alpha] mRNA over a 12 h time course experiment led us to inquire whether the extended elevation of transcripts involved Stx1induced mRNA stability. Our data suggest that the presence of Stx1 increases the stabilities of TNF-[alpha] and IL-1[beta] transcripts. In contrast to TNF-[alpha], the level of secreted IL-1[beta] protein does not correlate with the level IL-1[beta] mRNA, suggesting an alteration of post-translational processing and/or secretion of IL-1[beta]. Differentiated THP-1 cells produce chemokines in response to Stx1 and/or LPS treatments. Chemokines may enhance the destruction of tissue cells during an infection by mediating an inflammatory cell influx. Comparison of cytokine and chemokine mRNA and protein kinetics suggests that the regulation of expression may differ between individual cytokines and chemokines. Extension of experimental time courses demonstrated THP-1 cell sensitivity to killing by Stx1, especially in the presence of LPS. Further experiments revealed that undifferentiated and differentiated THP-1 cells were induced to undergo apoptosis following treatment with Stx1, LPS, and Stx1+LPS, and that caspase activation was involved. Collectively, these results allowed us to propose a model of the role of macrophages in Stx1 pathogenesis. Advisors/Committee Members: Tesh, Vernon L., McMurray, David N., Samuel, James E., Miranda, Rajesh.

Subjects/Keywords: Shiga toxin; cytokines; apoptosis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Harrison, L. M. (2004). The effects of Shiga toxin 1 on cytokine and chemokine production and apoptosis in a human monocytic cell line. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/1038

Chicago Manual of Style (16^th Edition):

Harrison, Lisa Margaret. “The effects of Shiga toxin 1 on cytokine and chemokine production and apoptosis in a human monocytic cell line.” 2004. Doctoral Dissertation, Texas A&M University. Accessed February 28, 2021. http://hdl.handle.net/1969.1/1038.

MLA Handbook (7^th Edition):

Harrison, Lisa Margaret. “The effects of Shiga toxin 1 on cytokine and chemokine production and apoptosis in a human monocytic cell line.” 2004. Web. 28 Feb 2021.

Vancouver:

Harrison LM. The effects of Shiga toxin 1 on cytokine and chemokine production and apoptosis in a human monocytic cell line. [Internet] [Doctoral dissertation]. Texas A&M University; 2004. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1969.1/1038.

Council of Science Editors:

Harrison LM. The effects of Shiga toxin 1 on cytokine and chemokine production and apoptosis in a human monocytic cell line. [Doctoral Dissertation]. Texas A&M University; 2004. Available from: http://hdl.handle.net/1969.1/1038

Texas A&M University

4. Skwor, Troy Arthur. The role of CCL5 (RANTES) in the immune response against Mycobacterium tuberculosis in the guinea pig.

Degree: PhD, Medical Sciences, 2005, Texas A&M University

URL: http://hdl.handle.net/1969.1/1506

► Tuberculosis is the second leading cause of morbidity and mortality worldwide due to an infectious disease. Development of a new tuberculosis (TB) vaccine would be… (more)

▼ Tuberculosis is the second leading cause of morbidity and mortality worldwide due to an infectious disease. Development of a new tuberculosis (TB) vaccine would be facilitated by a better understanding of the mechanisms of protection induced by the current TB vaccine, Mycobacterium bovis BCG. Recombinant guinea pig (rgp)CCL5 and anti-rgpCCL5 were developed and characterized. The biological activity of rgpCCL5 was determined in a chemotaxis assay using T lymphocytes and pleural exudate cells. The specificity of rabbit anti-rgpCCL5 polyclonal antibody was confirmed by Western blot. RgpCCL5 was used to stimulate alveolar and peritoneal macrophages in vitro. and cytokine/chemokine gene expression was evaluated using real-time PCR. RgpCCL5 stimulated TNFα, IL-1β, CCL2, and CXCL8 mRNA expression and TNFα protein production (as assessed in the L929 cell bioassay) in macrophages. The effect of BCG-vaccination on CCL5 expression and production in leukocytes infected with M. tuberculosis was examined in vitro and in vivo. Polyclonal anti-rgpCCL5 was used to develop an ELISA assay to quantify gpCCL5 protein levels, and real-time PCR was used to detect CCL5 mRNA. Leukocytes isolated from BCG-vaccinated guinea pigs and infected in vitro with virulent M. tuberculosis demonstrated significantly elevated gpCCL5 mRNA and protein compared to cells from naive animals. The response of gpCCL5 to M. tuberculosis in vivo was studied in tuberculous pleural effusions, where peak levels of CCL5 mRNA and protein were reached at day 4 post-induction. Disease severity, cellular differentiation, histology, and cytokine/chemokine mRNA levels in pleural cells and granulomas were analyzed on day 4 in guinea pigs induced with tuberculous pleurisy and treated with either rgpCCL5 or anti-rgpCCL5 by direct intra-pleural injection. In these studies, neutralizing CCL5 resulted in reduced macrophage accumulation, diminished levels of IFNγ, TNFα, and CCL5 mRNA in pleural effusion cells, and reduced spontaneous lymphocyte proliferation. Together these studies suggest an important role for gpCCL5 in activating leukocytes during M. tuberculosis infection. Advisors/Committee Members: McMurray, David (advisor), Welsh, Jane (committee member), Skare, Jonathon (committee member), Tesh, Vernon (committee member).

Subjects/Keywords: RANTES; chemokines; Mycobacterium tuberculosis; cytokines; pleurisy; macrophages

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APA (6^th Edition):

Skwor, T. A. (2005). The role of CCL5 (RANTES) in the immune response against Mycobacterium tuberculosis in the guinea pig. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/1506

Chicago Manual of Style (16^th Edition):

Skwor, Troy Arthur. “The role of CCL5 (RANTES) in the immune response against Mycobacterium tuberculosis in the guinea pig.” 2005. Doctoral Dissertation, Texas A&M University. Accessed February 28, 2021. http://hdl.handle.net/1969.1/1506.

MLA Handbook (7^th Edition):

Skwor, Troy Arthur. “The role of CCL5 (RANTES) in the immune response against Mycobacterium tuberculosis in the guinea pig.” 2005. Web. 28 Feb 2021.

Vancouver:

Skwor TA. The role of CCL5 (RANTES) in the immune response against Mycobacterium tuberculosis in the guinea pig. [Internet] [Doctoral dissertation]. Texas A&M University; 2005. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1969.1/1506.

Council of Science Editors:

Skwor TA. The role of CCL5 (RANTES) in the immune response against Mycobacterium tuberculosis in the guinea pig. [Doctoral Dissertation]. Texas A&M University; 2005. Available from: http://hdl.handle.net/1969.1/1506

Texas A&M University

5. Ly, Lan H. Immunosuppressive dietary n-3 polyunsaturated fatty acids differentially modulate costimulatory regulation of murine CD4+ T-cell function.

Degree: PhD, Nutrition, 2005, Texas A&M University

URL: http://hdl.handle.net/1969.1/1535

► Consumption of fish oils (FO) enriched with the n-3 polyunsaturated fatty acids (PUFA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), is beneficial to a variety… (more)

▼ Consumption of fish oils (FO) enriched with the n-3 polyunsaturated fatty acids (PUFA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), is beneficial to a variety of inflammatory disorders due, in part, to the alteration of membrane composition of T-lymphocytes and other immune cells. We previously observed that down-regulation of proliferation and cytokine synthesis by CD4+ T-cells in mice fed diets rich in n-3 PUFA was dependent on the involvement of CD28, a co-stimulatory molecule necessary for T-cell activation. Since the co-receptor homologues, CD28 and CTLA-4, have opposing effects on T-cell activation, we hypothesized that the balance of costimulatory and downregulatory properties of CD28 and CTLA-4, respectively, would be altered by diet. A significant increase (p<0.05) in CD28 and CTLA-4 surface expression was observed in CD4+ T-cells post-stimulation with phorbol ester and calcium ionophore (PMA/Iono) or anti-CD3 and anti-CD28 (αCD3/CD28) antibodies in all diet groups. A significant increase (p<0.01; 20%) in the number of CD28 molecules was observed in n-3 PUFA vs. CO-fed mice after 48 h of in vitro CD4+ T-cell activation, and both CTLA-4 mRNA transcript and protein levels were upregulated by 50% at 72 h post-activation (p<0.01). Treatment with anti-CTLA-4 mAb in vivo in Mycobacterium bovis (BCG)-vaccinated mice did not alter the suppressive effects of dietary n-3 PUFA on antigen (PPD)-induced lymphocyte proliferation or delayed hypersensitivity reactions. T-cells from both the C57BL/6 and IL-10mice fed dietary n-3 PUFA after 72 h of in vitro stimulation with αCD3/CD28. CD4T-cells from C57BL/6 mice fed DHA produced significantly less IFNγ and IL-10, while CD4T-cells from IL-10Ligation of CD28 upregulates IL-10 receptor (IL-10R) expression on CD4+ T-cells. Therefore, we hypothesized that dietary n-3 PUFA would suppress T-cell function through the effects of IL-10. Surprisingly, the proliferation of purified splenic CD4+ T-cells activated in vitro with αCD3/CD28 was suppressed by dietary n-3 PUFA in both conventional mice (C57BL/6) and IL-10 gene knockout (IL-10(-/-)) mice. Furthermore, IL-10R cell surface expression was significantly down-regulated on CD4+ T-cells from both the C67BL/6 and IL-10(-/-) mice fed dietary n-3 PUFA produced significantly more IFNγ compared to the CO-fed group. Advisors/Committee Members: Chapkin, Robert S. (advisor), Welsh, C. Jane (committee member), McMurray, David N. (committee member), Tesh, Vernon L. (committee member).

Subjects/Keywords: Mouse; Diet; T-lymphocytes; Immunity

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ly, L. H. (2005). Immunosuppressive dietary n-3 polyunsaturated fatty acids differentially modulate costimulatory regulation of murine CD4+ T-cell function. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/1535

Chicago Manual of Style (16^th Edition):

Ly, Lan H. “Immunosuppressive dietary n-3 polyunsaturated fatty acids differentially modulate costimulatory regulation of murine CD4+ T-cell function.” 2005. Doctoral Dissertation, Texas A&M University. Accessed February 28, 2021. http://hdl.handle.net/1969.1/1535.

MLA Handbook (7^th Edition):

Ly, Lan H. “Immunosuppressive dietary n-3 polyunsaturated fatty acids differentially modulate costimulatory regulation of murine CD4+ T-cell function.” 2005. Web. 28 Feb 2021.

Vancouver:

Ly LH. Immunosuppressive dietary n-3 polyunsaturated fatty acids differentially modulate costimulatory regulation of murine CD4+ T-cell function. [Internet] [Doctoral dissertation]. Texas A&M University; 2005. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1969.1/1535.

Council of Science Editors:

Ly LH. Immunosuppressive dietary n-3 polyunsaturated fatty acids differentially modulate costimulatory regulation of murine CD4+ T-cell function. [Doctoral Dissertation]. Texas A&M University; 2005. Available from: http://hdl.handle.net/1969.1/1535

Texas A&M University

6. Endicott-Yazdani, Tiana. Identification of Novel Salmonella Typhimurium Genes Required For Survival During Intestinal Inflammation.

Degree: PhD, Microbial & Molecular Pathogenesis, Texas A&M University

URL: http://hdl.handle.net/1969.1/154260

► Bovine ligated ileal loops provide the best model to examine Salmonella Typhimurium genes required for survival during the early stages of infection, as humans and… (more)

▼ Bovine ligated ileal loops provide the best model to examine Salmonella Typhimurium genes required for survival during the early stages of infection, as humans and cattle develop very similar intestinal pathogenesis in response to the organism. Utilizing pools of mutants, both single gene and multi-gene deletion mutants, much of the S. Typhimurium genome can be screened simultaneously. A library consisting of multi-gene deletion mutants was screened in ligated ileal loops in calves. Regions of the genome required for survival in this model were identified in mucus and tissue samples using microarray analysis. STM1187-90 was one such region identified as under selection in both mucus and tissue. A ASTM1188 mutant was confirmed to poorly colonize the intestinal mucus and tissue in the presence of inflammation in competitive infections with the wild type. Complementation in trans reversed the phenotype of the ASTM1188 mutant. The phenotype of the ASTM1188 mutant was replicated and complemented in trans in the murine colitis model. STM1188 is a Salmonella specific gene whose protein product we show to be located in the inner membrane. This gene is absent in host-adapted serovars S. Typhi and S. Paratyphi A. Mutation of the putative lipobox cysteine to alanine resulted in mis- localization of STM1188C24A to the cytoplasm, and the inability to complement ASTM1188 in trans in mice. A second screen of a single gene deletion pool (SGD) identified many novel genes with potential roles during inflammation as well as many predicted genes with defined roles during the early stages of infection. Several novel gene phenotypes were confirmed and subsequently complemented in competitive infections with wild type. AhilE was identified during SGD screening and confirmed in bovine ligated ileal loops as being selected against during competitive infections with extensive inflammation, however, it was not selected against when the inflammatory immune response was limited. HilE has been previously shown to negatively regulate SPI-1 expression. Utilizing the murine colitis model, the AhilE phenotype was confirmed and complemented during competitive infection with wild type. By using (3-galactosidase assays, AhilE was confirmed to overexpress SPI-1, however, surprisingly AhilE also overexpressed SPI-2 during SPI-1 inducing conditions. In the current studies we performed Salmonella screens in bovine ligated ileal loops and confirmed novel virulence genes required for survival during inflammation. Advisors/Committee Members: Adams, L. Garry (committee member), Skare, Jonathon (committee member), Tesh, Vernon (committee member), Andrews-Polymenis, Helene (committeechair).

Subjects/Keywords: Biomedical Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Endicott-Yazdani, T. (n.d.). Identification of Novel Salmonella Typhimurium Genes Required For Survival During Intestinal Inflammation. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/154260

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Chicago Manual of Style (16^th Edition):

Endicott-Yazdani, Tiana. “Identification of Novel Salmonella Typhimurium Genes Required For Survival During Intestinal Inflammation.” Doctoral Dissertation, Texas A&M University. Accessed February 28, 2021. http://hdl.handle.net/1969.1/154260.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

MLA Handbook (7^th Edition):

Endicott-Yazdani, Tiana. “Identification of Novel Salmonella Typhimurium Genes Required For Survival During Intestinal Inflammation.” Web. 28 Feb 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Endicott-Yazdani T. Identification of Novel Salmonella Typhimurium Genes Required For Survival During Intestinal Inflammation. [Internet] [Doctoral dissertation]. Texas A&M University; [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1969.1/154260.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Council of Science Editors:

Endicott-Yazdani T. Identification of Novel Salmonella Typhimurium Genes Required For Survival During Intestinal Inflammation. [Doctoral Dissertation]. Texas A&M University; Available from: http://hdl.handle.net/1969.1/154260

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Texas A&M University

7. Nayak, Mamatha Somanath. Theiler's virus-induced apoptosis in cerebrovascular endothelial cells.

Degree: PhD, Biology, 2004, Texas A&M University

URL: http://hdl.handle.net/1969.1/347

► Theiler's murine encephalomyelitis virus (TMEV) is classified as a Cardiovirus in the Picornaviridae family. An enteric virus, TMEV, spreads within the mouse population by the… (more)

▼ Theiler's murine encephalomyelitis virus (TMEV) is classified as a Cardiovirus in the Picornaviridae family. An enteric virus, TMEV, spreads within the mouse population by the fecal-oral route. The neurovirulent GDVII strain of Theiler's virus causes a fatal encephalitis in all strains of mice following intra-cranial infection of the virus. Persistent BeAn strain of Theiler's virus causes a demyelinating disease in susceptible strains of mice, which is similar to the human disease - Multiple Sclerosis (MS). Although a well-recognized model for MS, the route of entry of the virus into the central nervous system (CNS) following natural infection has not been well understood. One of the proposed portals of entry includes the blood-brain barrier (BBB). This report indicates the ability of both the neurovirulent and the persistent strains of Theiler's virus to induce apoptosis in the functional units of the BBB - the cerebrovascular endothelial cells (CVE) both in vitro and in vivo. Induction of apoptosis in CVE was demonstrated by Annexin staining, electron microscopy, DNA fragmentation assay, Hoechst staining and by caspase-3 staining. Corresponding to results by other authors, GDVII is a stronger inducer of apoptosis in CVE compared to BeAn. Induction of apoptosis is dependent on the MOI of the virus. UV-inactivated virus is not capable of inducing apoptosis and induction of apoptosis appears to be an internal event not requiring activation of death receptors. Determining the pathway of induction of apoptosis by TMEV in CVE indicated the involvement of a Ca2+ dependent pathway for apoptosis - the calpain pathway. Involvement of calpain in apoptosis has been reported in MS. Induction of apoptosis in CVE in vivo was also demonstrated following the intra-peritoneal inoculation of Theiler's virus. Induction of apoptosis in CVE following Theiler' virus infection could lead to a breach of the BBB and entry of inflammatory cells as well as virus into the central nervous system. This finding could aid understanding the neuropathogenesis of Theiler's virus. Advisors/Committee Members: Welsh, Cristabel J. (advisor), Moyes, Rita J. (advisor), Tiffany-Castiglioni, Evelyn (committee member), Tesh, Vernon L. (committee member), Miranda, Rajesh C. (committee member).

Subjects/Keywords: Theiler's virus; Apoptosis; Cerebrovascular endothelial cells; Multiple Sclerosis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nayak, M. S. (2004). Theiler's virus-induced apoptosis in cerebrovascular endothelial cells. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/347

Chicago Manual of Style (16^th Edition):

Nayak, Mamatha Somanath. “Theiler's virus-induced apoptosis in cerebrovascular endothelial cells.” 2004. Doctoral Dissertation, Texas A&M University. Accessed February 28, 2021. http://hdl.handle.net/1969.1/347.

MLA Handbook (7^th Edition):

Nayak, Mamatha Somanath. “Theiler's virus-induced apoptosis in cerebrovascular endothelial cells.” 2004. Web. 28 Feb 2021.

Vancouver:

Nayak MS. Theiler's virus-induced apoptosis in cerebrovascular endothelial cells. [Internet] [Doctoral dissertation]. Texas A&M University; 2004. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1969.1/347.

Council of Science Editors:

Nayak MS. Theiler's virus-induced apoptosis in cerebrovascular endothelial cells. [Doctoral Dissertation]. Texas A&M University; 2004. Available from: http://hdl.handle.net/1969.1/347

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