Evaluating the Anti-Tumor Efficacy of a Bacterial Immunomodulatory Protein in a Murine Model
Transcription
Begin with an anesthetized female mouse in a supine position, bearing urothelial tumors in its bladder epithelium.
Secure the hind legs, locate the urethral opening, and insert a catheter into the mouse's bladder. Wash the bladder to remove urine.
Inject Helicobacter pylori neutrophil-activating protein, or HP-NAP — an immunomodulatory bacterial protein.
In the tumor microenvironment, HP-NAP interacts with Toll-like receptors on neutrophils and initiates a signaling cascade, increasing proinflammatory cytokine expression.
The cytokines trigger the differentiation of naÏve T lymphocytes into type 1 T helper, or Th1, and type 1 cytotoxic, or Tc1, lymphocytes that produce interferon-gamma.
Interferon-gamma inhibits new blood vessel formation, limiting nutrient and oxygen availability to the tumor.
Additionally, it upregulates tumor-antigen-presenting MHC molecules on the tumor cells, facilitating interaction with Tc1 cells.
This interaction results in the release of cytotoxic molecules that induce tumor cell death, demonstrating the anti-tumor efficacy of HP-NAP.
