States » SouthPosted at: Oct 25 2026 12:13PM


RGCB scientists uncover new pathway for spread of pneumonia toxin between cells

Thiruvananthapuram, Oct 25 (UNI) Scientists at the BRIC–Rajiv Gandhi Centre for Biotechnology (RGCB) here have identified a previously unrecognised mechanism through which a toxin produced by pneumonia-causing bacteria can spread from one cell to another, potentially extending tissue damage during infection.
The study, published in the Journal of Extracellular Vesicles, reveals how the body's cellular repair mechanism, intended to protect damaged cells, may inadvertently facilitate the transfer of pneumolysin, a potent toxin produced by Streptococcus pneumoniae, to neighbouring cells.
The researchers found that when cells respond to damage caused by the toxin, they release tiny membrane-bound structures called extracellular microvesicles. These vesicles can retain biologically active pneumolysin and transport it to adjacent cells, creating an additional pathway for toxin-mediated damage.
Pneumolysin is a pore-forming toxin that binds to cholesterol in cell membranes and creates openings that compromise their integrity. When exposed to sub-lethal levels of the toxin, cells attempt to limit the damage by shedding affected portions of their plasma membranes through the release of extracellular vesicles.
The RGCB team discovered that pneumolysin becomes concentrated in these membrane-derived microvesicles and remains biologically active instead of being eliminated as cellular waste. The toxin-bearing vesicles can subsequently interact with neighbouring cells and cause further membrane damage.
Molecular simulations conducted in collaboration with Dr Jagannath Mondal and colleagues at the Tata Institute of Fundamental Research (TIFR), Hyderabad, revealed a previously unrecognised mechanism through which an exposed region of vesicle-bound pneumolysin engages lipids in the recipient cell membrane.
This interaction promotes membrane bending and thinning, while facilitating water penetration into the membrane. Altering key amino acids involved in the interaction substantially reduced membrane deformation, supporting the role of this mechanism beyond the toxin's conventional pore-forming activity.
The researchers also demonstrated the process using human cells. Microvesicles released by monocytes exposed to pneumolysin transferred the toxin to human peripheral blood immune cells, compromised their membrane integrity and increased cell death.
Cryo-electron microscopy (Cryo-EM) analysis, carried out in collaboration with Dr Somnath Dutta and colleagues at the Indian Institute of Science (IISc), Bengaluru, helped reveal the localisation of pneumolysin at sites of membrane interaction.
Senior researcher Dr Karthik Subramanian said the findings highlighted an unexpected consequence of the host cell's own repair machinery.
A process intended to protect a damaged cell can effectively repackage pneumolysin into another membrane-active form, enabling toxin-bearing microvesicles to interact with neighbouring cells and extend damage beyond the initially affected cell, he explained.
The findings offer fresh insights into the mechanisms through which pneumococcal infections may cause cellular and tissue damage. They also highlight the complex interaction between bacterial toxins and the host body's defence and repair responses.
However, further studies, including investigations in living organisms, will be needed to establish the contribution of this pathway to disease progression and determine whether blocking microvesicle-mediated toxin transfer could offer a potential therapeutic approach.
The study opens a new avenue for research into how bacterial toxins spread within tissues and how the body's cellular responses might influence the course of infection.
UNI DS
Tags: #RGCB scientists uncover new pathway for spread of pneumonia toxin between cells
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