Francisella tularensis, the bacterium causing tularemia, is usually studied in immune cells, but gene editing in these cells is challenging, leading researchers to explore HeLa epithelial cells instead.
A new model using HeLa cells expressing mouse FcγRII (HeLa-FcγRII) was developed, showing a significant increase in infection rates of F. novicida, up to 100 times more than regular HeLa cells.
Gene silencing experiments revealed that knocking down GLS1 (glutaminase) in HeLa-FcγRII cells increased cell death during infection, suggesting that ammonia produced from glutaminase is crucial for F. novicida's growth.
The bacterium causing tularemia is highly harmful to humans and can grow inside immune cells while suppressing the host’s immune response.
Researchers conducted a large-scale study using a library of mutant strains to find 13 mutants that increased TNF-α production in infected macrophages, identifying 10 genes, including 6 new ones, linked to immunosuppression.
One gene, associated with the pyrimidine biosynthesis pathway, showed that its deletion led to increased TNF-α and other immune responses, suggesting a connection between this gene and the bacterium's ability to suppress the immune system through the STING pathway.
The study focuses on identifying factors that help the tularemia-causing bacteria survive and grow within arthropods, specifically using a silkworm infection model.
Researchers screened a library of transposon mutants and found that the MltA protein is crucial for bacterial growth in silkworms.
The absence of MltA led to reduced bacterial numbers and heightened immune responses in silkworms, indicating its role in both insect and potential human pathogenicity.
Francisella tularensis is a highly dangerous bacteria responsible for tularemia that suppresses host immune responses while growing inside cells, but how it does this is not well understood.
Researchers created a library of transposon mutants of F. tularensis to discover new factors involved in its pathogenicity, isolating 11 strains that showed reduced cytotoxicity.
One specific gene, slt, was found crucial for cytotoxicity; a mutant lacking this gene was less harmful to human cells and had trouble surviving inside them, leading to increased immune response compared to the wild-type strain.*