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  1. Home
  3. Group A Streptococcal Collagen-like Protein 1 Restricts Tumor Growth In Murine Pancreatic Adenocarcinoma And Inhibits Cancer-promoting Neutrophil Extracellular Traps.
  1. Home
  3. Group A Streptococcal Collagen-like Protein 1 Restricts Tumor Growth In Murine Pancreatic Adenocarcinoma And Inhibits Cancer-promoting Neutrophil Extracellular Traps.

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Group A streptococcal collagen-like protein 1 restricts tumor growth in murine pancreatic adenocarcinoma and inhibits

Emily A Henderson1, Abby Ivey2, Soo Jeon Choi1

  • 1Department of Microbiology, Immunology and Cell Biology, School of Medicine, West Virginia University, Morgantown, WV, United States.

Frontiers in Immunology
|March 22, 2024

View abstract on PubMed

Summary
This summary is machine-generated.
Keywords:
bacteriotherapygroup A Streptococcusmyeloperoxidaseneutrophil extracellular trapspancreatic cancer

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Intra-tumoral injection of Group A Streptococcus (GAS) reduced pancreatic cancer growth by inhibiting neutrophil extracellular traps (NETs). The streptococcal collagen-like protein 1 (Scl1) was key to this anti-tumor effect, offering a novel therapeutic strategy.

Area of Science:

  • Immunology
  • Oncology
  • Microbiology

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) is characterized by an immunosuppressive tumor microenvironment.
  • Neutrophil extracellular traps (NETs) contribute to immune tolerance in PDAC and represent a therapeutic target.
  • Group A Streptococcus (GAS) possesses mechanisms to inhibit NET formation.

Purpose of the Study:

  • To investigate the potential of intra-tumoral GAS injection as a strategy to stimulate anti-tumor immunity in PDAC.
  • To assess the role of streptococcal collagen-like protein 1 (Scl1) in mediating anti-PDAC activity and NET inhibition.

Main Methods:

  • Murine PDAC models (Panc02 and KPC) were treated with intra-tumoral injections of different M-type GAS strains.
  • Tumor growth, bacterial colonization, systemic spread, and humoral immune responses were evaluated.
  • The role of Scl1 was assessed using wild-type, Scl1-deficient, and complemented GAS strains, alongside in vitro/ex vivo NET inhibition assays.

    • Main Results:

    • Intra-tumoral GAS injection significantly reduced pancreatic tumor volume in both PDAC models.
    • Tumor growth inhibition was dependent on Scl1, with Scl1-deficient strains showing no effect.
    • Scl1 inhibited NET formation in vitro and ex vivo, and its presence localized GAS to the tumor, limiting systemic spread.

    Conclusions:

    • Intra-tumoral GAS injection is a viable strategy for reducing PDAC growth.
    • The Scl1 protein facilitates anti-PDAC activity, partly by inhibiting cancer-promoting NETs.
    • Targeting NETs via Scl1 presents a novel therapeutic approach for pancreatic cancer.