One of the most remembered facts from biology class is about mitochondria. They’re called the “powerhouse of the cell” because they help make energy. But new research published in Cell reveals another crucial role. Mitochondria also help your immune system detect and trap harmful bacteria.
Inside neutrophils, a type of white blood cell, mitochondria act as sensors. They detect a chemical called lactate, which is made by bacteria during infection. When mitochondria sense lactate, they send a signal inside the neutrophil. This signal tells the neutrophil to launch a defense called a NET.
NETs, or neutrophil extracellular traps, are sticky webs made of DNA and proteins. These webs trap bacteria and help stop them from spreading. Scientists once thought NETs only formed from stress or damage inside cells. But this study shows NETs can also form in response to bacterial activity.
The discovery shows that mitochondria do more than make energy. They help your immune system respond to threats and fight off infection.
How Do Mitochondria Trigger NET Formation?
When neutrophils engulf bacteria, they trap them inside a compartment. Inside this compartment, bacteria release a chemical called lactate. Neutrophils detect this lactate using a special transporter called MCT1. This transporter moves the lactate from the compartment to the mitochondria.
Inside the mitochondria, lactate is broken down into pyruvate. This process creates stress signals, including reactive oxygen species, or free radicals. These signals tell the neutrophil to release a NET to trap the bacteria. If this signaling fails, the neutrophil cannot launch an effective immune response.
Researchers blocked lactate use with special inhibitors. When blocked, mitochondria failed to send the signals needed to form NETs.
They also tested neutrophils from patients with systemic lupus erythematosus, or SLE. SLE is an autoimmune disease that attacks healthy tissues and weakens the immune response. In SLE neutrophils, mitochondria stored less energy and activated poorly. These neutrophils absorbed lactate but couldn’t convert it to pyruvate.
Without this conversion, the mitochondria made fewer free radicals. These radicals are needed to trigger NET release and immune defense.
When healthy neutrophils were given the same inhibitor, they also failed to form NETs. But they still formed NETs in response to dead cell debris. This shows that SLE-related NET formation follows a different path than bacterial NET formation. SLE neutrophils cannot detect bacterial lactate, so they cannot trap bacteria. As a result, people with SLE may be more likely to develop serious infections.
What New Treatments Could This Discovery Lead to?
This study points to new ways to treat infection and immune disorders. New treatments may help neutrophils trap bacteria in people with low immunity. That includes people with autoimmune diseases or chronic infections.
But in some diseases, NETs can do more harm than good. Too many NETs may damage tissues, as seen in lupus and COVID-19. In these cases, blocking mitochondrial sensing could reduce harm. This may help prevent the immune system from attacking the body.
Researchers also wonder if other immune cells detect bacterial by-products. It’s possible that other signals, besides lactate, help trigger immune defenses. Future studies may uncover new ways to control these responses. That could lead to better treatments with fewer side effects.
Conclusion
Mitochondria help neutrophils sense bacteria and launch targeted immune traps. This discovery reveals new ways to treat both infection and autoimmune disorders. Boosting or blocking this response could protect people with different immune needs.
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Logan Hamilton is a health and wellness freelance writer for hire. He’s passionate about crafting crystal-clear, captivating, and credible content that elevates brands and establishes trust. When not writing, Logan can be found hiking, sticking his nose in bizarre books, or playing drums in a local rock band. Find him at loganjameshamilton.com.
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