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PA-MSHA promotes antitumor immunity in STK11 mutant NSCLC through activating the STING pathway of immune cells

Guofang Yin1, Fang He1, Qiusha Guo1

  • 1Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China; Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.

International Immunopharmacology
|May 3, 2026
PubMed
Abstract

Insights

Pseudomonas aeruginosa mannose-sensitive-hemagglutinin (PA-MSHA) enhances immune cell activity against STK11-mutant non-small cell lung cancer (NSCLC). This immunotherapy approach activates the STING pathway, offering a novel strategy for this treatment-resistant cancer.

Area of Science:

  • Immunology
  • Oncology
  • Microbiology

Background:

  • Serine/threonine kinase 11 (STK11) mutant non-small cell lung cancer (NSCLC) is characterized by a "cold" tumor immune microenvironment (TIME), leading to primary resistance to immunotherapy.
  • Patients with STK11 mutations have limited benefit from current immunotherapies, necessitating the development of alternative therapeutic strategies.

Purpose of the Study:

  • To investigate the potential of Pseudomonas aeruginosa mannose-sensitive-hemagglutinin (PA-MSHA) as a therapeutic agent for STK11-mutant NSCLC.
  • To elucidate the mechanisms by which PA-MSHA impacts the tumor immune microenvironment and enhances anti-tumor immunity.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) and flow cytometry analysis (FCA) were used to assess PA-MSHA's impact on immune cells.
  • Cell viability, colony formation, immunofluorescence staining, western blot, and proteomics analyses were performed to investigate anti-tumor effects and mechanisms.
  • A cell-derived xenograft (CDX) model with human peripheral blood mononuclear cells (PBMCs) was utilized for in vivo studies.

Main Results:

  • PA-MSHA enhanced the cytotoxic activity of immune cells (THP-1 and Jurkat) against STK11-mutant NSCLC cells in vitro.
  • In vivo, PA-MSHA combined with sintilimab significantly inhibited tumor growth in a CDX model.
  • PA-MSHA induced an immune-responsive TIME, reprogrammed immune cell phenotypes, and promoted cytotoxic functions, associated with upregulated STING expression and pathway activation.

Conclusions:

  • PA-MSHA demonstrates potential in improving immune cell function and enhancing anti-tumor effects against STK11-mutant NSCLC.
  • The observed therapeutic benefits are mechanistically linked to the activation of the stimulator of interferon genes (STING) pathway.
Keywords:
ImmunotherapyNSCLCPA-MSHASTINGSTK11TIME

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