The molecular mechanisms of listeriolysin O-induced lipid membrane damage Original paper
Researched by:
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Divine Aleru
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Divine Aleru
Read MoreI am a biochemist with a deep curiosity for the human microbiome and how it shapes human health, and I enjoy making microbiome science more accessible through research and writing. With 2 years experience in microbiome research, I have curated microbiome studies, analyzed microbial signatures, and now focus on interventions as a Microbiome Signatures and Interventions Research Coordinator.
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Microbes
Microbes
Microbes are microscopic organisms living in and on the human body, shaping health through digestion, vitamin production, and immune protection. When microbial balance is disrupted, disease can occur. This guide explains key microbe types—bacteria, viruses, fungi, protozoa, and archaea—plus major pathogenic and beneficial examples.
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Divine Aleru
Read More
Researched by:
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Divine Aleru
ID
Divine Aleru
Read More
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Divine Aleru
What was studied?
The study explores the role of listeriolysin O (LLO), a cholesterol-dependent cytolysin produced by Listeria monocytogenes, in the pathogen’s ability to invade host cells, disrupt membranes, and facilitate intracellular survival. The focus is on LLO’s interactions with lipid membranes, its pore-forming mechanism, and its influence on the host immune response.
Who was studied?
The study primarily investigates the bacterial virulence factor Listeriolysin O (LLO) in the context of Listeria monocytogenes infection, examining its role in membrane damage and intracellular activities.
What were the most important findings?
LLO is integral to Listeria monocytogenes‘ ability to disrupt host cell membranes and propagate intracellularly. The toxin functions by forming pores in host cell membranes, specifically targeting cholesterol-rich lipid bilayers. The mechanism involves the binding of LLO to membranes, oligomerization into arc-shaped complexes, and insertion into the lipid membrane to create functional pores of varying sizes. These pores facilitate the escape of Listeria from phagosomes, enabling bacterial replication in the cytosol. The activity of LLO is highly pH-dependent and regulated by factors such as cholesterol availability in the host cell membranes. This regulation ensures that the toxin does not cause excessive damage to the bacterial replicative niche. The presence of specific structural motifs in LLO, such as the PEST-like sequence, contributes to its degradation and prevents excessive cytotoxicity, promoting bacterial survival and limiting host damage during infection.
What are the greatest implications of this study?
Understanding LLO’s role in bacterial pathogenesis provides insights into the molecular mechanisms of Listeria monocytogenes infection. This knowledge is crucial for developing therapeutic strategies targeting LLO or its membrane-binding activity. By targeting LLO, it may be possible to reduce the pathogen’s ability to invade host cells and replicate intracellularly, potentially leading to more effective treatments for listeriosis. Additionally, the study suggests that LLO could be harnessed in biotechnology and medical applications, such as vaccines or drug delivery systems, due to its potent immunogenic properties and ability to selectively target cellular membranes.
Listeria monocytogenes
Listeria monocytogenes is an opportunistic pathogen capable of surviving in diverse environments, including soil, water, and decaying vegetation. L. monocytogenes has the unique ability to evade the immune system by moving directly from cell to cell within the host. This intracellular lifestyle allows the bacterium to avoid extracellular immune detection, contributing to its ability to cause invasive diseases like meningitis and septicemia, particularly in the elderly and immunocompromised.