Researchers at the Ecole Polytechnique Federale de Lausanne (EPFL) have uncovered a striking mechanism by which the bacteria that cause tuberculosis assemble into thread-like cords. This cord formation appears to push on the nuclei inside lung cells and alters how the immune system responds. The findings, published in Cell, could steer future drug development aimed at tuberculosis treatment.
Historical observations noted that the tuberculosis bacterium tends to form cord-like structures, a pattern seen for decades. In the current study, scientists used a cutting-edge platform called lungs on a chip to watch the very first moments of infection. This technology makes it possible to visualize how bacteria meet host cells at the air-liquid interface within the lungs, revealing that cord formation begins early in the infection process. Experiments conducted in mice corroborated this early development, reinforcing the relevance of the observation across species.
The team also mapped how these bacterial threads interact with the cell nucleus, the repository of genetic material. The mechanical forces generated by the cords appear to influence the way cells regulate immune responses, suggesting that physical interactions between pathogens and host cells may shape disease outcomes in tuberculosis beyond purely chemical signaling.
As the authors note, the broader scientific community is increasingly recognizing that mechanical cues play a significant role in cellular behavior and immune activity. Traditional cell culture systems often fail to recreate the native mechanical environment of tissues, so the new findings highlight an important gap that dynamic, physiologically relevant models can fill.
Beyond observing structure, the study explores how the threads maintain their integrity and resist antibiotic treatment. The researchers propose that treating tuberculosis could benefit from viewing the bacteria as a collective system, rather than as isolated units. Such a shift in perspective could help tailor therapies that disrupt cord formation and resilience, potentially reducing the reliance on high-dose antibiotics while improving treatment effectiveness.
In related context, prior scientific work has shown that antibodies can be designed to mimic genetic mutations that protect against neurodegenerative conditions. These parallel lines of inquiry underscore the broader potential of immune-focused strategies and molecular approaches to combat complex diseases, including tuberculosis, dementia, and other chronic conditions. The new tuberculosis study thus sits at a nexus of microbiology, immunology, and bioengineering, offering a richer picture of how organisms adapt to and manipulate their host environments.