Scientists have discovered how Mycobacterium tuberculosis hardens immune cell membranes to survive in the body. This is a breakthrough achievement that could lead to the development of new tuberculosis treatments.
Researchers have discovered an advanced biophysical trick that allows us to: tuberculosis– Allows bacteria to survive inside human cells, potentially leading to new treatments for diseases.
Tuberculosis, which kills more than 1 million people each year, continues to pose a major public health challenge, particularly in Asia, Africa, and Latin America. The disease is caused by mycobacteria, microorganisms that have evolved strategies 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.”
Vesicles that harden immune cells
new research It shows that mycobacteria release small packages known as extracellular vesicles. These vesicles fuse with the membranes of immune cells and contain specialized lipids.
Normally, immune cells trap harmful bacteria in compartments called phagosomes, which then fuse with lysosomes.
Normally, immune cells trap harmful bacteria in compartments called phagosomes, which then fuse with lysosomes. The researchers discovered that mycobacteria prevent this fusion by stiffening the phagosomal membrane, effectively building a protective bunker inside human cells.
“When the membrane becomes stiffer, it becomes much more difficult for phagosomes to fuse with lysosomes,” Panda says. “This is an elegant biophysical mechanism: bacteria rebuild their membrane structures to escape the very processes that kill them.” The researchers also found that the vesicles are not restricted to infected cells, but can weaken surrounding immune cells even before they encounter the bacteria.
Mycobacteria have evolved sophisticated ways to hijack human immune cells and avoid destruction. Specifically, it strengthens the inner membrane and prevents the digestive enzymes within the lysosomes from destroying the bacteria.
Lipid-centered approach
This discovery points to a new way to understand mycobacterial survival. While previous research has focused primarily on the proteins that bacteria destroy, this study focuses on the important role of lipids. Introduction of bacterial lipids into host cell membranes is sufficient to cause 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.
Impact beyond tuberculosis
Researchers have observed similar extracellular vesicle-mediated membrane stiffening effects in other pathogens, including: Klebsiella pneumoniae and Staphylococcus aureussuggesting that this may be an evolutionarily conserved strategy.
Now that you know how bacteria protect themselves, you can start looking for ways to stop them.
The discovery could have major implications for potential treatments, as scientists may be able to target proteins involved in vesicle production or counteract the membrane-stiffening effect, allowing immune cells to function normally.
“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.”