TEHRAN (ISNA)- An Iranian researcher Nader Ghasemlou jointly with his colleagues at Boston Children's Hospital has found out that the pain of invasive skin infections caused by methicillin-resistantStaphylococcus aureus, and possibly other serious, painful infections, appear to be induced by the invading bacteria themselves, and not by the body's immune response as previously thought.
What's more, their research demonstrates that once the pain neurons "sense" the bacteria, they suppress the immune system, potentially helping the bacteria become more virulent.

The study, conducted in a mouse model and published online by the journal Nature could change the way doctors think about a variety of invasive, painful infections, such as meningitis, necrotizing fasciitis, urinary tract infections, dental caries and intestinal infections.

"If we could block pain in infected tissues and also block what pain neurons do to the immune system, it could help us treat bacterial infections better," said Isaac Chiu, PhD, the study's first author.

The study was launched after Chiu and coauthor Christian A. Von Hehn, MD, PhD, were culturing sensory neurons and immune cells together in a dish to see how they interact during an infection. "Surprisingly, the neurons were responding immediately to the bacteria," said Chiu.

Bacteria "talk to neurons"

The research showed that S. aureus bacteria secrete two kinds of compounds that communicate with sensory neurons, inducing pain:

� N-formyl peptides: Pain neurons carry receptors to detect these peptides, known as FPR1 receptors, the team demonstrated. When mice are unable to make these receptors, they show a reduced pain response.

� Pore-forming toxins: These proteins, also secreted by other virulent bacteria, dock on the sensory nerve terminals and create large pores that let ions into the cells�triggering them to fire off pain messages. A pore-forming toxin known as alpha toxin is known to help S. aureus spread in the skin and lungs.

These findings suggest possible new approaches for blocking pain signaling by blocking the FPR1 receptor, blocking the receptor for alpha-toxin (ADAM10) on sensory neurons or possibly delivering a drug through the pores. These approaches also might prevent the neurons from suppressing the immune response, Chiu says, but this has yet to be proven.

The study was supported by the National Institutes of Health.

By ISNA

 

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