Antibiotics are designed to kill harmful bacteria and help the body recover from infection. But some antibiotics may also push bacteria to release tiny particles that can make inflammation worse.

While inflammation is part of the body’s natural defense against infection, too much inflammation can damage healthy tissue and interfere with healing. In severe cases, excessive inflammation can become life-threatening.

These particles are called bacterial extracellular vesicles, or BEVs. These microscopic, bubblelike structures carry proteins, toxins and other molecular signals that influence how the immune system of the host responds. Bacteria naturally release BEVs into their surroundings as a way to communicate with their environment, remove damaged cellular material and interact with host cells.

Although incredibly small, these structures can have powerful effects on the human body. When BEVs enter the bloodstream, they can interact with cells that line blood vessels and trigger an immune response. In some cases, this can increase inflammation and lead to sepsis, a condition where the body’s response to infection becomes dangerously uncontrolled, damaging tissues and sometimes leading to organ failure.

I am a biomedical engineer studying how bacterial extracellular vesicles influence inflammation during infection. In my recently published research, I found that certain types of antibiotic cause bacteria to release significantly more of these vesicles than others. This finding suggests that the way an antibiotic kills bacteria may also influence how much inflammatory material is released into the body.

When antibiotics stress bacteria

Antibiotics work in different ways. Some target the bacterial cell wall, weakening it until the cell breaks apart and dies. Others interfere with key cellular processes such as protein production or DNA replication, preventing bacteria from growing. Whatever their mechanism, antibiotics control infection by killing the bacteria that are causing it.

But antibiotics also place bacteria under stress, and that stress can cause bacteria to release more extracellular vesicles carrying inflammatory molecules. To explore this process, I exposed the bacteria E. coli to several commonly used antibiotics and measured how many vesicles they made. The goal was simple: Compare how different types of antibiotics influence vesicle release and determine whether the way an antibiotic kills bacteria affects vesicle production.

The results showed that not all antibiotics have the same effect on the vesicles bacteria produce.

Antibiotics that target the bacterial cell wall, including a widely used group of drugs known as beta-lactams, led to a noticeable increase in vesicle production. In contrast, antibiotics that act on protein or DNA processes showed a much smaller effect.

This difference likely reflects how bacteria respond to damage. When the bacteria’s cell wall is disrupted, bacteria may release more vesicles as a way to shed damaged material or adapt to stress. The inflammatory molecules these vesicles carry can further activate the body’s immune response.

This raises an important question: Could some antibiotics unintentionally amplify inflammation and make an infection worse?

My findings do not show that antibiotics directly contribute to infections, but they do suggest that antibiotic type could potentially influence not only how effectively bacteria are killed but also how the body responds to the infection. More research is needed to understand how these bacterial responses affect patients during severe infections, such as sepsis.

Why this matters for treating infections

It is important to emphasize that antibiotics remain one of the most effective and lifesaving tools in modern medicine. This research does not suggest they should be avoided. Instead, it highlights that bacteria are not passive targets. They actively respond to treatment, and those responses can have additional effects on the body.

Understanding how bacteria react to antibiotics could help researchers and clinicians better evaluate how different treatments influence both infection and inflammation. In situations where controlling inflammation is critical, such as severe infections, these differences may become especially important.

This work also reflects a broader shift in how scientists think about infection. Rather than focusing only on killing bacteria, researchers are increasingly studying how bacteria communicate, respond to stress and interact with the human body.

As scientists continue to uncover how bacteria behave under antibiotic pressure, it becomes clear that treating infection is not only about stopping bacterial growth but also about understanding the signals bacteria leave behind.

Panteha Torabian receives funding from NIH.