Honors Program

Midway Honors, Honors in Biology

Date of Award


Thesis Professor(s)

Tammy R. Ozment

Thesis Professor Department


Thesis Reader(s)

David L. Williams,Thomas Laughlin


Sepsis is the body’s response to an overwhelming infection and is a serious consequence of critical illness. It can cause tissue damage, organ failure, and death. Sepsis continues to have an unacceptably high mortality rate, due to the lack of effective treatments. Specific therapeutic targets for sepsis remain elusive since the complex functional changes that result in a septic state remain poorly understood. Macrophage Scavenger Receptor A (SRA, CD204) is a surface receptor that binds negatively charged, endogenous and exogenous ligands. We have discovered that SRA plays a significant role in the pathophysiology of sepsis. We have shown that mice with SRA have increased inflammation, decreased survival, and increased bacterial burden compared to SRA deficient mice. We have also found an increase in the expression of SRA on monocytes and macrophages in septic wild type mice. To determine the mechanism responsible for increased SRA expression in sepsis we treated a mouse macrophage cell line, (J774a.1), with mediators that stimulate toll like receptors (TLRs), innate immune receptors which are activated in sepsis. The cells were cultured with ultra pure LPS (a TLR 4 ligand), PAM3CSK4 (a TLR 2 ligand), glucan (a Dectin-1 ligand), ultra pure LPS and PAM3CSK4, or ultra pure LPS and glucan for 24 hours. The cells were stained with an SRA antibody, and flow cytometry was used to measure the SRA expression for each treatment group. LPS treatment alone resulted in a significant increase in SRA expression when compared to control cells. Specifically, LPS increased SRA expression by 53.4% compared to media alone (p


East Tennessee State University

Document Type

Honors Thesis - Open Access

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.


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