Poster Presentation Lorne Infection and Immunity 2023

Streptococcus pneumoniae potently kill mesothelial and mesothelioma cells in a strain dependent manner (#193)

Hui Juin Shak 1 2 3
  1. Pleural Medicine Unit, Institute for Respiratory Health, Perth, WA, Australia
  2. School of Medicine, The University of Western Australia, Perth, WA, Australia
  3. Respiratory Medicine, Sir Charles Gairdner Hospital, Perth, WA, Australia

Introduction & Aims: Mesothelioma is a fatal cancer and there is no cure for it. Chemotherapy

treatment has shown only minor improvement in survival and current standard treatment is

mainly palliative. The use of bacteria or their products presents an attractive approach in

mesothelioma as there is strong evidence to suggest that bacterial infection in the pleura may

increase survival in these patients. In this preliminary study, we aimed to assess the killing

capacity of Streptococcus pneumoniae against mesothelioma cells.

Methods: Clinical S. pneumoniae strains (n= 10) collected from patients with invasive bacterial

infection were co-cultured with patient-derived mesothelioma cells (n=9) and benign

mesothelial cell line (MeT-5A). S. pneumoniae strains at concentration of 1×107 and 1×104

CFU/mL were added to confluent mesothelioma/mesothelial cells. Cell viability at 0, 4 and 8

hours post infection was assessed by flow cytometry using a Live/Dead cell viability assay.

 

Results: Our data show a high variability in the mesothelioma/mesothelial cells killing by clinical

S. pneumoniae strains, where some strains have a high killing capacity towards some cells, but

not the others. For example, on HAM cell line, one bacterial strain killed up to 83% cells while

other strain only killed 9.2% of the cells at 4 hours, despite having the same starting inoculum.

S. pneumoniae strains increase killing of the five mesothelioma cell lines by median of 1.9 to

9.44-fold over controls at 4 hours, and by 1.67 to 15.19-fold at 8 hours. The fold change varies

significantly, between cell lines and bacterial strains.

 

Conclusion:

Understanding the mechanisms underlying the inter-strain variability may provide insight for

future therapeutic approaches for mesothelioma.