Cholera bacteria form aggressive biofilm on immune cells

Bacteria have discovered the power of communities. A group of researchers from the University of Basel in Switzerland has made an intriguing discovery about the bacterial pathogen responsible for cholera. They found that this bacterium forms a unique type of bacterial community on immune cells, specifically an aggressive biofilm that proves lethal for the cells. This study, recently published in the journal Cell, provides fresh insights into the infection strategies employed by pathogens.

Biofilms, which are communities of bacteria that form on surfaces, present a captivating defense mechanism. We come across biofilms in our everyday lives, such as dental plaque in our mouths, slimy films on water stones, or even as part of our intestinal flora. Bacterial biofilms possess inherent tolerance to antibiotics, making them particularly dangerous in clinical settings when they colonize implants, catheters, or surgical instruments.

This colonization allows pathogens to invade our bodies and initiate infections that are challenging for both the immune system and antibiotics to combat.

Until now, it was believed that bacteria formed biofilms primarily for self-defense and protection. However, the research team led by Prof. Knut Drescher at the Biozentrum, University of Basel, has recently demonstrated, in their study published in Cell, that bacteria can form biofilms on the surfaces of immune cells. This previously unknown type of community differs from previously known bacterial biofilms not only in its structure but also in its function: instead of serving a protective purpose, this biofilm exhibits aggressive behavior.

Biofilm on immune cells: meshwork rather than typical slimy matrix

Drescher’s team has made a groundbreaking discovery regarding a new form of biofilm found in Vibrio cholerae, the bacterium responsible for causing cholera. This particular pathogen has the ability to colonize various immune cells within the human host.

In order to gain a deeper understanding of how biofilms form on immune cells, the researchers focused their attention on a specific type of phagocytic cell known as macrophages. According to Lucia Vidakovic, the first author of the study, when bacteria come into contact with a macrophage by chance, they attach themselves to the cell’s surface using a “feeler” of sorts. Following this initial attachment, the bacteria begin to divide and intertwine their feeler-like appendages.

The structure of the extracellular matrix in this unique biofilm significantly differs from previously known biofilms, where bacteria are typically embedded within a slimy matrix composed of sugars and proteins.

Biofilms on immune cells are an aggressive instead of defensive strategy

As time passes, the biofilms created by the cholera pathogen progressively envelop macrophages, resulting in their demise. Lucia Vidakovic explains, “The bacterial community actively assaults and kills the immune cells. However, we initially lacked a clear understanding of the precise mechanism.” To unravel this puzzle, the team meticulously investigated all 14 known toxins produced by the cholera pathogen and ultimately pinpointed the hemolysin as the culprit.

This toxin forms pores in the protective membrane of the immune cells, leading to their death.

Cholera, a highly dangerous infectious disease characterized by severe diarrhea, solely affects humans as the host for the cholera pathogen. To study this phenomenon, the scientists established a model using human intestinal organoids. Through this model, they were able to demonstrate that Vibrio cholerae can form lethal biofilms on macrophages after colonizing and disrupting the human intestinal barrier.

Knut Drescher adds, “This innovative attack strategy employed by the bacteria can significantly impact the progression of cholera infection. In our next phase, we aim to investigate whether other pathogens also form such aggressive biofilms. Understanding the tactics employed by bacterial pathogens is crucial for developing new approaches to combat them.”

Source: University of Basel

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