Role of Borrelia Burgdorferi Infection in Normal Breast Cell Metabolic Reprogramming and Warburg Phenotype Development

Date of Submission

8-2025

Document Type

Thesis

Degree Name

Master of Science in Cellular and Molecular Biology

Department

Biology and Environmental Sciences

Advisor

Eva Sapi, Ph.D.

Committee Member

Alireza G. Senejani, Ph.D.

Committee Member

Martha Anne Taddeo Ph.D.

Keywords

Lyme disease, Borrelia burgdorferi, Warburg Effect, Tumorigenesis, Metabolic Reprogramming, Brest Epithelial Cells

LCSH

Lyme disease, Borrelia burgdorferi, Carcinogenesis, Breast, Epithelial cells, Ixodes scapularis

Abstract

Lyme disease, caused by Borrelia burgdorferi, is a growing concern in the United States and traditionally presents with a bull’s eye rash and flu-like symptoms following a tick bite. Emerging research suggests that B. burgdorferi can also induce cancer formation, or tumorigenesis. Various pathogens can drive tumorigenic changes through means of inducing a metabolic shift in normal cells, a phenomenon known as the Warburg effect - a hallmark of cancer. While there is evidence of B. burgdorferi triggering Warburg effect in immune cells, its impact on normal breast epithelial cells remains unclear. This thesis investigated whether B. burgdorferi infection can trigger Warburg-like metabolic reprogramming in MCF10A cells using short term (up to 72h) and prolonged infections (18 weeks). Changes in glycolytic metabolism and gene expression were evaluated using a glucose uptake assay and quantitative real-time PCR for Warburg effect related genes. The glucose uptake assay revealed a significant increase in glucose uptake after the 24 and 72 hours marks, as well as after 18 weeks. Short term infections resulted in a significant downregulation of HK2, with no significant changes in GLUT1, PFKM or HIF1A expression. In contrast, prolonged infections caused a significant upregulation of HK2, PFKM and HIF1A. These findings suggest that B. burgdorferi infections can induce metabolic changes in normal epithelial breast cells, particularly inducing the Warburg Effect. This raises the possibility that chronic bacterial infections may contribute to early cancer development by reprogramming host cell metabolism. Understanding the link between B. burgdorferi infections and cancer development can greatly benefit future clinical research strategies pertaining to early detection and prevention of cancer formation in patients initially bitten by Ixodes ticks.

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