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News
Researchers at Juntendo University have uncovered a lipid signaling pathway — the 12-HHT/BLT2 axis — that helps epithelial cells patch up membrane damage caused by bacterial toxins. When toxins punch holes in cells, calcium floods in, triggering 12-HHT production, which activates BLT2 to kick off two repair strategies: shedding damaged membrane bits and reinforcing the cell's internal skeleton. The findings open a new door for host-directed therapies against bacterial infections.
Bacteria have a nasty trick: they produce pore-forming toxins that drill holes into cell membranes, causing cells to leak vital contents and die. But it turns out our cells aren't defenseless — researchers at Juntendo University have identified a built-in emergency repair system that helps epithelial cells survive these attacks.
The study, published in the Journal of Cell Biology, zeroes in on the 12-HHT/BLT2 signaling axis. When toxins punch holes in the membrane, calcium rushes in, triggering production of 12-HHT — a bioactive lipid. That lipid activates the BLT2 receptor, which then launches two coordinated repair responses: cells pinch off damaged membrane sections (including the toxin pores themselves) into tiny bubbles called extracellular vesicles, and they reorganize their internal actin scaffolding via Rac1 to shore up structural integrity. Cells with enhanced BLT2 signaling showed significantly better survival, while those lacking BLT2 were far more likely to rupture and die.
Key Takeaways:
Why it matters: Rather than solely targeting the pathogen, this discovery suggests a complementary strategy — boosting the host cell's own repair machinery. That could be especially valuable for infections where antibiotic resistance is a growing concern.
