A new method could change the future of treating drug-resistant infections

 

Researchers have developed a new and exciting way to combat drug-resistant infections, based on boosting the body's immune system

Researchers have developed a new and exciting way to combat drug-resistant infections, based on boosting the body's immune system.

Antimicrobial resistance (AMR) is one of the world’s most serious health threats, in which bacteria, viruses, fungi and parasites lose their ability to respond to drug treatments. 

Common drug-resistant infections include urinary tract infections, pneumonia, Escherichia coli (E. coli), methicillin-resistant Staphylococcus aureus (MRSA), and Clostridium difficile. This problem has been exacerbated globally by the scarcity of new antibiotics developed in recent decades.

The new approach is based on a different idea than traditional methods, as it does not seek to kill microbes directly, but rather to "train" the body's immune cells, especially macrophages, to become more efficient in fighting infection.

Researchers at Trinity College Dublin have succeeded in achieving this by exposing these cells to a natural protein called "interferon gamma," which is part of the body's immune response when exposed to infection.

The results showed that after this "training" the phagocytic cells became faster and more effective at killing bacteria, including dangerous bacteria such as drug-resistant Staphylococcus aureus, as well as tuberculosis bacteria.

Phagocytic cells are the immune system's first line of defense, engulfing and destroying microbes before they can spread throughout the body. When enhanced with interferon gamma, their ability to respond quickly and eliminate pathogens more efficiently is increased.

The study's lead researcher, Deirbla Murphy of Trinity College Dublin, says the cells "became more capable of killing tuberculosis bacteria and Staphylococcus aureus after being trained."

This discovery builds on previous research on tuberculosis and COVID-19 vaccines, which showed that interferon gamma plays a crucial role in activating immune-related genes. It has also been observed that individuals who received the tuberculosis vaccine were less likely to die from various infections, not just tuberculosis.

Researchers are now trying to mimic this protective effect without the need for a vaccine, by boosting what is known as "innate immunity," which is the body's rapid line of defense that responds to any threat in a general way without forming long-term immune memory.

This is different from the "adaptive immunity" that vaccines rely on, which learns how to recognize specific pathogens and builds a long-term immune memory against them.

Researchers hope this approach will enhance the body's ability to resist a wide range of infections, including bacterial, fungal, and viral ones, and not just one type.

The research team also tested this method on cells from patients with genetic mutations that increase their susceptibility to infection, and succeeded in improving their immune response in the laboratory.

The next steps involve testing the possibility of using this "immunological training" to treat additional types of infections, such as fungi and viruses.

Researchers hope that this method will be used in the future as an adjunctive treatment alongside current antibiotics, especially in cases of resistant infections.

It is worth noting that interferon gamma is already used in some hospitals and given intravenously to treat severe conditions such as sepsis.

However, experts caution that these findings are still in their early stages. Immunologist Jenna Machioki says the study is "biologically sound," but remains limited to laboratory experiments.

She adds that over-activating the immune system can lead to inflammation or tissue damage, and may also increase the risk of exacerbating some autoimmune diseases.

Nevertheless, researchers believe this approach may represent a promising new direction in medicine, known as "host-targeted therapies," which focuses on helping the body itself fight infection rather than directly targeting the microbe.



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