Publication Date

2016

Document Type

Thesis

Committee Members

Nancy J. Bigley (Advisor), Barbara E. Hull (Committee Member), Dawn P. Wooley (Committee Member)

Degree Name

Master of Science (MS)

Abstract

Macrophages play a crucial role for our immune system and protect our body from infection. Suppressor of cytokine signaling (SOCS) proteins negatively regulate cytokine receptor and TLRs. The aryl hydrocarbon receptor (AhR) also performs an important role in immunity. This study investigated the changes in expression of AhR in RAW 264.7 macrophage cells after the addition of SOCS1 and SOCS3 peptide mimetics and also examined AhR expression in RAW 264.7 macrophage cells before and after the addition of HSV-1 RAW 264.7 murine macrophage cell lines which are from male BALB/c mice were used in this study. The addition of the SOCS1 peptide mimetic treatment of uninfected RAW 264.7 macrophages caused a significant increase in AhR expression (p<0.001) associated with production of the pro-inflammatory cytokines such as TNF-a. However, treatment of uninfected RAW 264.7 macrophages with SOCS3 peptide mimetic caused a significant decrease in AhR expression compared to uninfected control cells (p<0.01) associated with production of IL-10. Following viral challenge, there was an overall decrease in AhR expression in all treated RAW 264.7 macrophages. During the course of the study, viabilities of RAW 264.7 macrophages with and without HSV-1 were assessed. Treatment of macrophages with SOCS3 increased cell viability compared to SOCS1 treatment while viability following both treatments was reduced in virus infected cells. These observations suggest that SOCS3 plays a critical role in controlling the effect of cytotoxic molecules. This study shows that SOCS1 peptide and SOCS3 peptide mimetic can impact AhR expression and cell survival of murine macrophages.

Page Count

65

Department or Program

Microbiology and Immunology

Year Degree Awarded

2016

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