The mycobacteria that cause tuberculosis harden their cell membranes to avoid destruction, but this discovery opens a new avenue for treatment..

Three important points of RT:

1. Membrane hardening survival strategy: The bacteria that cause tuberculosis release extracellular vesicles filled with lipids that harden the immune cell membrane and prevent the fusion of phagosomes and lysosomes, allowing the bacteria to survive inside the cell.
2. Immune dysfunction caused by lipids: This study reveals a new lipid-centered mechanism of immune evasion and shows that bacterial lipids alone can physically alter host cell membranes and weaken immune defenses, even in nearby uninfected cells.
3. new therapeutic targets: By identifying vesicle generation and membrane stiffening as important survival tools, the findings suggest new therapeutic strategies aimed at blocking these processes and allowing immune cells to effectively clear infections.

Scientists have discovered an elegant biophysical trick. Bacteria that cause tuberculosis The discovery could lead to new strategies to fight one of the world’s deadliest infectious diseases.

Tuberculosis kills more than one million people each year and remains a major public health crisis, particularly in Asia, Africa and Latin America. This disease is caused by mycobacteria. Mycobacteria have evolved sophisticated ways to hijack human immune cells and avoid destruction.

“Tuberculosis is endemic in India,” said Ayush Panda, a former graduate student in Mohammed Saleem’s lab at India’s National Institute of Science Education and Research. “I grew up in a state where tuberculosis outbreaks are a big problem, and I’ve always been interested in how these diseases spread. That’s what drew me to this research.”

The research content to be announced at 70th Annual Meeting of the Biophysical Society (February 21-25, 2026, San Francisco)recently posted BioRxivit was revealed that mycobacteria release small packages called extracellular vesicles that fuse with the membranes of immune cells. These vesicles contain special lipids (fat molecules) that make cell membranes more rigid.

Normally, when our immune cells engulf harmful bacteria, they become trapped in a compartment called a phagosome, which then fuses with another compartment called a lysosome. Lysosomes contain digestive enzymes that break down and destroy bacteria. However, the researchers discovered that mycobacteria prevent this fusion from occurring by stiffening the phagosomal membrane, essentially building a protective bunker around itself inside our cells.

“When the membrane becomes stiffer, it becomes much more difficult for phagosomes to fuse with lysosomes,” Panda explained. “This is an elegant biophysical mechanism: bacteria rebuild their membrane structures to escape the very process that kills them.” The researchers also discovered that these vesicles are not restricted to infected cells. It can affect nearby immune cells, weakening them even before they come into contact with bacteria.

What makes this discovery particularly important is that it represents an entirely new way to understand how mycobacteria survive. Previous research has focused primarily on proteins that bacteria destroy. This study takes a lipid-centric approach and shows that the introduction of bacterial lipids into host cell membranes is sufficient to induce immune dysfunction.

“The most surprising finding was that when we introduced mycobacterial lipids into membranes that mimic host phagosomes, we observed significant physical changes. The properties of the membranes changed completely,” Panda said.

Researchers also observed similar extracellular vesicle-mediated membrane effects. Klebsiella pneumoniae and Staphylococcus aureussuggesting an evolutionarily conserved strategy among pathogens. This discovery opens up several promising avenues for developing new treatments. Researchers may be able to target the proteins involved in the production of these bacterial vesicles or find ways to counteract the membrane-stiffening effect.

“Now that we know how bacteria protect themselves, we can start looking for ways to stop them,” Panda says. “If we can prevent the bacteria from hardening the membrane, our immune cells may be able to function and stop the infection.”