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You searched for +publisher:"Temple University" +contributor:("Ho, Wen-zhe;"). Showing records 1 – 2 of 2 total matches.

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Temple University

1. Zhou, Yu. HCV, Heroin Use, and MicroRNAs.

Degree: PhD, 2014, Temple University

Pathology

Hepatitis C virus (HCV) infection is common among injection drug users (IDUs). There is accumulating evidence that circulating microRNAs (miRNAs) are related to HCV infection and disease progression. The present study was undertaken to determine the in vivo impact of heroin use on HCV infection and HCV-related circulating miRNA expression. Using the blood specimens from four groups of study subjects (HCV-infected individuals, heroin users with/without HCV infection, and healthy volunteers), we found that HCV- infected heroin users had significantly higher viral load than HCV-infected non-heroin users (p=0.0004). Measurement of HCV-related circulating miRNAs in plasma showed that miRs-122, 141, 29a, 29b, and 29c were significantly increased in the heroin users with HCV infection, whereas miR-351, an HCV inhibitory miRNA, was significantly decreased in heroin users as compared to control subjects. Further investigation identified a negative correlation between the plasma levels of miR-29 family members and severity of HCV infection based on aspartate aminotransferase to platelet ratio index (APRI). Heroin use and/or HCV infection also dysregulated a panel of plasma miRNAs. Taken together, these data for the first time revealed in vivo evidence that heroin use and/or HCV infection alter circulating miRNAs, which provides a novel mechanism for the impaired innate anti-HCV immunity among IDUs. Recent studies revealed that extracellular miRNAs were able to incorporate into cell-derived exosomes as a method of cell-to-cell interaction. Exosomes are a class of cell-released small vesicles that mediate intercellular communication by delivering functional factors to recipient cells. During HCV infection, the interaction between liver resident macrophages and hepatocytes is important for host defense and viral elimination, triggered by innate immune activation, especially Toll like receptors (TLR). In our study, we explored the role of macrophage-derived exosomes in the transmission of innate immune responses against HCV infection in hepatocytes, and the involvement of exosomal miRNAs in transferring the anti-HCV activities. We reported that upon TLR3 activation, macrophages shed exosomes that were able to attenuate HCV-JFH1 infection in Huh7 cells. We further demonstrated that exosomes from poly I:C treated macrophages were internalized by Huh7 cells, which induced the intercellular anti-HCV responses (type I interferon, interferon stimulated genes, etc.) and thus drastically inhibited HCV infection in Huh7 cells. Moreover, using an in vitro macrophage and Huh7 cell co-culture model, we also found exosomes mediated HCV suppression in Huh7 cells after TLR3 activation. The presence of exosome inhibitor in co-culture compromised the anti-HCV activity by TLR3-activated macrophages. Interestingly, the miRNA-29 family, which was reported to suppress HCV infection, was significantly increased in the macrophage exosomes after TLR3 activation. The inhibition of miRNA-29 partially compromised the anti-HCV activity of…

Advisors/Committee Members: Ho, Wen-zhe;, Ramirez, Servio, Kolson, Dennis L., Shore, Scott K., Rawls, Scott M.;.

Subjects/Keywords: Biology; Microbiology; Immunology;

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

APA (6th Edition):

Zhou, Y. (2014). HCV, Heroin Use, and MicroRNAs. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,309425

Chicago Manual of Style (16th Edition):

Zhou, Yu. “HCV, Heroin Use, and MicroRNAs.” 2014. Doctoral Dissertation, Temple University. Accessed November 26, 2020. http://digital.library.temple.edu/u?/p245801coll10,309425.

MLA Handbook (7th Edition):

Zhou, Yu. “HCV, Heroin Use, and MicroRNAs.” 2014. Web. 26 Nov 2020.

Vancouver:

Zhou Y. HCV, Heroin Use, and MicroRNAs. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Nov 26]. Available from: http://digital.library.temple.edu/u?/p245801coll10,309425.

Council of Science Editors:

Zhou Y. HCV, Heroin Use, and MicroRNAs. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,309425


Temple University

2. Breslow, Jessica. Effect of Morphine on Immune Responses and Infection.

Degree: PhD, 2010, Temple University

Microbiology and Immunology

Opioids have been shown to modulate immune function in a variety of assays and animal models. In a more limited number of studies, opioids have been shown to sensitize to infection. Heroin, the prototypical opioid drug of abuse, is rapidly metabolized to morphine in the body. Morphine has been used as an analgesic for hundreds of years, and continues to be a drug of choice for treating pain in ICU and trauma patients. The continued use of these opioid compounds in humans warrants further investigation of their effect on immune responses against, and progression of, common bacterial infections. Two infections were investigated in this thesis using murine models, Acinetobacter baumannii and Salmonella typhimurium. A recent increase in the prevalence of A. baumannii infections among healthy, but wounded, military personnel, lead to the hypothesis that analgesic morphine might sensitize to infection with this multiply-drug resistant bacterium. A systemic, intraperitoneal A. baumannii infection model was established in mice that resulted in rapid, disseminated disease where animals became septic as organisms replicated in the blood, lungs, and other organs. This model was used to investigate the role of various parameters of innate immune defenses to Acinetobacter. Neutralization of neutrophils by antibody depletion greatly sensitized to this infection. Infection resulted in a rapid, biphasic induction of both IL-17 and the chemokine, KC/CXCL1, a major chemotactic factor for neutrophils, that continued to rise through 18h after bacterial inoculation. However, depletion of either IL-17 or KC/CXCL1 using monoclonal antibodies failed to sensitize to Acinetobacter infection. Further, IL-17 receptor KO mice were not sensitized to this infection. Collectively, these results suggest that there must be other chemotactic factors for neutrophils that can compensate for the absence of IL-17 and KC. Morphine, delivered by extended release pellet, sensitized two strains of mice to two strains of Acinetobacter, as measured by mortality to a sublethal challenge dose, and this effect was blocked by administration of the opioid-receptor antagonist, naltrexone. . Morphine increased Acinetobacter burdens in the organs and blood of infected mice, and increased the levels of pro-inflammatory cytokines. Evidence for an effect of morphine on neutrophil infiltration was obtained. Morphine decreased the total numbers of cells, as well as the total numbers of neutrophils and macrophages infiltrating into the peritoneal cavity. This inhibition of neutrophil accumulation correlated with suppression of levels of both IL-17 and KC/CXCL1. The evidence supports the conclusion that morphine sensitizes to Acinetobacter infection by suppressing the response of neutrophils, potentially via depression of neutrophil chemotactic factors IL-17 and KC. However, taken together with the data above there are probably additional factors in addition to IL-17 and KC that are sensitizing the animals to infection in…

Advisors/Committee Members: Eisenstein, Toby K., Adler, Martin W., Buttaro, Bettina A., Ho, Wen-zhe, Monestier, Marc.

Subjects/Keywords: Microbiology; Acinetobacter baumannii; Immunity; Infection; Morphine; Opioids; Salmonella enterica serovar Typhimurium

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

APA (6th Edition):

Breslow, J. (2010). Effect of Morphine on Immune Responses and Infection. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,103429

Chicago Manual of Style (16th Edition):

Breslow, Jessica. “Effect of Morphine on Immune Responses and Infection.” 2010. Doctoral Dissertation, Temple University. Accessed November 26, 2020. http://digital.library.temple.edu/u?/p245801coll10,103429.

MLA Handbook (7th Edition):

Breslow, Jessica. “Effect of Morphine on Immune Responses and Infection.” 2010. Web. 26 Nov 2020.

Vancouver:

Breslow J. Effect of Morphine on Immune Responses and Infection. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2020 Nov 26]. Available from: http://digital.library.temple.edu/u?/p245801coll10,103429.

Council of Science Editors:

Breslow J. Effect of Morphine on Immune Responses and Infection. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,103429

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