Publication Date


Document Type


Committee Members

Nancy Bigley (Advisor), Julian Cambronero (Committee Member), Barbara Hull (Committee Member)

Degree Name

Master of Science (MS)


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.

Page Count


Department or Program

Microbiology and Immunology

Year Degree Awarded