Mitochondria were mainly known as the energy production components cells. But scientists are more and more discovered That these small organelles do much more than power cells. They are also involved in immune functions such as control inflammation,, regulate cell death And Respond to infections.
Search for my colleagues and I revealed that the mitochondria play another Key role in your immune response: detect bacterial activity and help neutrophils, a type of white blood cells, trap them and kill them.
Over the past 16 years, My research has concentrated On understanding the decisions that immune cells take during the infection and the way in which the degradation of these decision -making processes leads to a disease. The recent conclusions of my laboratory highlight why people with Autoimmune diseases As lupus may find it difficult to fight infections, revealing a potential link between Dysfunctional mitochondria and weakened immune defenses.
Secret weapons of the immune system
Neutrophils are the most abundant immune cell type and serve as immune system first speakers. One of their main defense mechanisms is to release Extracellular traps or netrophiles – Weblike structures composed of DNA and antimicrobial proteins. These sticky nets trap and neutralize the invading microbes, preventing their spread in the body.
Until recently, scientists thought that net training was mainly triggered by stress and cell damage. However, our study revealed that mitochondria can detect a specific bacterial by -product – lactate – and use this signal to initiate net training.
Lactate is generally associated with Muscle fatigue in people. But in the context of bacterial infectionsHe plays a different role. Many bacteria release lactate As part of their own energy production. My team discovered that once bacteria are swallowed up by a cell compartment called the phagosomeNeutrophils can detect the presence of this lactate.
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Inside the phagosome, this lactate communicate to neutrophils that bacteria are present and antibacterial processes are not sufficient to kill these pathogens. When mitochondria in neutrophil cells detect this lactate, they Start signaling So that the cell gets rid of the nets that have trapped bacteria. Once bacteria have been released outside the cell, other immune cells can kill them.
When we blocked the capacity of mitochondria to feel lactate, neutrophils Failure of the production of nets effectively. This meant that bacteria were more likely to escape capture and proliferate, showing how crucial this mechanism is for immune defense. This process highlights a complex dialogue between the metabolism of bacteria and the energy cells of the host cell.
What makes this discovery surprising is that mitochondria in cells are capable of detecting bacteria trapped in phagosomes, even if the microbes are locked in a separate space. In one way or another, mitochondrial sensors can collect signals inside these compartments – an impressive exploit of cellular coordination.
Target mitochondria to fight against infections
Our study is part of an increasing field called immunostabolismexploring how metabolism and the immune function is deeply linked. Rather than considering cellular metabolism as strictly a means of generating energy, researchers now recognize it as a central engine of immune decisions.
The mitochondria are seated at the heart of this interaction. Their ability to feel, respond and even shape the metabolic environment of a cell gives them a critical role To determine how and when the immune responses are deployed.
For example, our results provide a key reason why patients with chronic autoimmune disease called Systemic lupus erythematosus often suffer from recurring infections. Mitochondria in neutrophils of lupus patients Do not feel the bacterial lactate correctly. Consequently, net production has been considerably reduced. This mitochondrial dysfunction could explain why lupus patients are more vulnerable to bacterial infections – even if their immune system is constantly activated due to the disease.
This observation indicates the central role of mitochondria in the balance of immune responses. It links two apparently independent problems: immune overactivity, as shown by lupus, and immune weakness as an increased sensitivity to infection. When the mitochondria work properly, they help neutrophils to set up an effective and targeted attack against bacteria. But when the mitochondria is altered, this system is broken down.
Our discovery that mitochondria can feel bacterial lactate to trigger net training opens up new possibilities for processing infections. For example, drugs that improve mitochondrial detection could stimulate net production in people with weakened immune systems. On the other hand, for the conditions where the net contributes to tissue lesions – as in severe COVVI -19 or autoimmune diseases – it may be advantageous to limit this response.
In addition, our study raises the question of whether other immune cells use similar mechanisms to detect microbial metabolites, and other bacterial by-products could serve as immune signals. Understanding these more detail routes could lead to new treatments that more precisely modulate immune responses, reducing collateral damage while preserving antimicrobial defenses.
The mitochondria are not only the powers of the cell – these are the watchtowns of the immune system, even the lowest metabolic signals of the bacterial invaders. As the understanding of researchers from their roles extends, we also appreciate the complexity – and adaptability – of our cellular defenses.
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