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You searched for +publisher:"Temple University" +contributor:("Kolson, Dennis L."). Showing records 1 – 2 of 2 total matches.

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Temple University

1. Gerngross, Lindsey. TARGETING CFMS SIGNALING TO RESTORE IMMUNE FUNCTION AND ERADICATE HIV RESERVOIRS.

Degree: PhD, 2015, Temple University

Biomedical Neuroscience

While combination anti-retroviral therapy (cART) has improved the length and quality of life of individuals living with HIV-1 infection, the prevalence of HIV-associated neurocognitive disorders (HAND) has increased and remains a significant clinical concern. The neuropathogenesis of HAND is not completely understood, however, latent HIV infection in the central nervous system (CNS) and chronic neuroinflammation are believed to play a prominent role. CNS-associated macrophages and resident microglia are significant contributors to CNS inflammation and constitute the chief reservoir of HIV-1 infection in the CNS. Previous studies from our lab suggest monocyte/macrophage invasion of the CNS in HIV may be driven by altered monocyte/macrophage homeostasis. We have reported expansion of a monocyte subset (CD14+CD16+CD163+) in peripheral blood of HIV+ patients that is phenotypically similar to macrophages/microglia that accumulate in the CNS as seen in post-mortem tissue. The factors driving the expansion of this monocyte subset are unknown, however, signaling through cFMS, a type III receptor tyrosine kinase (RTK), may play a role. Macrophage-colony stimulating factor (M-CSF), a ligand of cFMS, has been shown to be elevated in the cerebral spinal fluid (CSF) of individuals with the most severe form of HAND, HIV-associated dementia (HAD). M-CSF promotes a Macrophage-2-like phenotype and increases CD16 and CD163 expression in cultured monocytes. M-CSF has also been shown to increase the susceptibility of macrophages to HIV infection and enhance virus production. These findings, in addition to the known function of M-CSF in promoting macrophage survival, supports a role for M-CSF in the development and maintenance of macrophage viral reservoirs in tissues where these cells accumulate, including the CNS. Interestingly, a second ligand for cFMS, IL-34, was recently identified and reported to share some functions with M-CSF, suggesting that both ligands may contribute to HIV-associated CNS injury and AIDS pathogenesis. Through immunohistochemical studies using a relevant animal model of HIV infection, SIV infected rhesus macaques, we reported the presence of M-CSF and IL-34 in the brains of seronegative and SIV+ animals, for the first time, and identified spatial differences in the expression of these ligands. Important to our interest in viral persistence in the CNS, we observed the predominance of M-CSF expression in brain to be by cells that comprise perivascular cuffs and nodular lesions, which contain monocytes/ macrophages that have migrated into the CNS. IL-34 appeared to be a tissue-specific ligand expressed by resident microglia. Like M-CSF, we found that IL-34 also increased the frequency of CD16+CD163+ monocytes in vitro. We further investigated the potential of cFMS inhibition as a means to abrogate macrophage-2-like immune polarization using the small molecule tyrosine kinase inhibitor (TKI), GW2580. The addition of GW2580 abolished cFMS ligand-mediated increases in CD16+CD163+ monocyte…

Advisors/Committee Members: Fischer-Smith, Tracy;, Rappaport, Jay, Langford, Dianne, Kolson, Dennis L., Wigdahl, Brian;.

Subjects/Keywords: Nanoscience

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

APA (6th Edition):

Gerngross, L. (2015). TARGETING CFMS SIGNALING TO RESTORE IMMUNE FUNCTION AND ERADICATE HIV RESERVOIRS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,286848

Chicago Manual of Style (16th Edition):

Gerngross, Lindsey. “TARGETING CFMS SIGNALING TO RESTORE IMMUNE FUNCTION AND ERADICATE HIV RESERVOIRS.” 2015. Doctoral Dissertation, Temple University. Accessed October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,286848.

MLA Handbook (7th Edition):

Gerngross, Lindsey. “TARGETING CFMS SIGNALING TO RESTORE IMMUNE FUNCTION AND ERADICATE HIV RESERVOIRS.” 2015. Web. 30 Oct 2020.

Vancouver:

Gerngross L. TARGETING CFMS SIGNALING TO RESTORE IMMUNE FUNCTION AND ERADICATE HIV RESERVOIRS. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Oct 30]. Available from: http://digital.library.temple.edu/u?/p245801coll10,286848.

Council of Science Editors:

Gerngross L. TARGETING CFMS SIGNALING TO RESTORE IMMUNE FUNCTION AND ERADICATE HIV RESERVOIRS. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,286848


Temple University

2. 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 October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,309425.

MLA Handbook (7th Edition):

Zhou, Yu. “HCV, Heroin Use, and MicroRNAs.” 2014. Web. 30 Oct 2020.

Vancouver:

Zhou Y. HCV, Heroin Use, and MicroRNAs. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Oct 30]. 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

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