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The Effects of HSV-1 Challenge on Polarized Murine Macrophages: an In Vitro Model Using the J774A.1 Murine Macrophage Cell Line

Reichard, Adam Craig

Abstract Details

2012, Master of Science (MS), Wright State University, Microbiology and Immunology.
In our current study we examined the effects of HSV-1 challenge on J774A.1 macrophages polarized to either a proinflammatory (M1) or anti-inflammatory (M2) phenotype. Polarized J774A.1 macrophages were characterized using CD14-CD86 and SOCS1-SOCS3 expression levels. SOCS proteins are a family of proteins that are capable of inhibiting cytokine-signaling pathways. HSV-1 up regulates expression of SOCS1 protein levels in infected cells, inhibiting the ability of infected cells to produce proinflammatory products (Nowoslawski Akhtar and Benveniste, 2011). This study shows that signals within the microenvironment play a greater role in macrophage polarization, and SOCS1-SOCS3 expression levels, than does HSV-1 challenge. M1 macrophages showed morphological changes following polarization, a significant decrease in cell viability, a two-fold increase in the number of CD14+-CD86+ cells, similar levels of SOCS1 expression, and a 11-fold decrease in SOCS3 expression when compared to control cells. M2 macrophages also exhibited morphological changes, a slight decrease in cell viability, a 26.0% decrease in the number of CD14+-CD86+ cells, and SOCS1-SOCS3 expression levels similar to that of control cells. Following HSV-1 challenge (0.1 MOI), the majority of M1 macrophages and M2 macrophages appeared rounded, possibly due to disruption of actin filaments. Virus-infected M1 macrophages showed a slight decrease in cell viability when compared to uninfected M1 macrophages. Additionally, the number of CD14+-CD86+ cells of both M1 and M2 phenotypes decreased. M1 macrophages exhibited a 39.9% decrease, while M2 macrophages exhibited a 13.2% decrease. SOCS1 expression levels remained relatively unchanged in virus-infected M1 macrophages, while SOCS3 expression levels increased by 30.4% at 24 hours after infection. Increase in SOCS3 levels is hypothesized to be a protective response of infected M1 macrophages due to the release of high levels of proinflammatory molecules. Alternatively, the SOCS1-SOCS3 ratio remained relatively unchanged in the anti-inflammatory phenotype.
Nancy Bigley, PhD (Advisor)
Barbara Hull, PhD (Committee Member)
Julian Cambronero, PhD (Committee Member)
77 p.

Recommended Citations

Citations

  • Reichard, A. C. (2012). The Effects of HSV-1 Challenge on Polarized Murine Macrophages: an In Vitro Model Using the J774A.1 Murine Macrophage Cell Line [Master's thesis, Wright State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=wright1343411395

    APA Style (7th edition)

  • Reichard, Adam. The Effects of HSV-1 Challenge on Polarized Murine Macrophages: an In Vitro Model Using the J774A.1 Murine Macrophage Cell Line. 2012. Wright State University, Master's thesis. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=wright1343411395.

    MLA Style (8th edition)

  • Reichard, Adam. "The Effects of HSV-1 Challenge on Polarized Murine Macrophages: an In Vitro Model Using the J774A.1 Murine Macrophage Cell Line." Master's thesis, Wright State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1343411395

    Chicago Manual of Style (17th edition)