A recent study published in the journal Nature Communications discovered, on the molecular level, how bacterial infections could cause toothaches.
Bacterial infections, particularly ones with Gram-negative bacteria, cause major human diseases such as pneumonia, meningitis, gastroenteritis and gonorrhea. Gram-negative bacteria are dangerous due to its most significant disease-causing feature, lipopolysaccharide (LPS), which lies in its outer wall.
When someone contracts a bacterial infection, LPS fragments from damaged parts of the bacterial wall are released nearby and then trigger an immune response. When these bits meet up with a certain type of receptor, it induces a chemical reaction involved in immune function, which leads to swelling, tissue injury and the bacteria's destruction.
The human immune system is not fast-acting in response to LPS, but for some reason, fast reactions like acute pain, inflammation and low blood pressure were occurring in its presence. This study, led by author Victor M. Meseguer (UC Berkeley), proves why.
Meseguer had a toothache and was told that it was because of a bacterial infection, but the details on the molecular level that led to this diagnosis were yet unknown. So he and researchers dug deeper and found that it was caused by bacterial LPS targeting TRPA1, an immune cell receptor.
LPS inserted into the membrane surrounding sensory nerve endings causes a mechanical deformation that is then sensed by TRPA1 proteins. This leads to almost instantaneous activation of TRPA1, which, combine with the rush of positively-charged ions into the nerves and the firing of electric signals, is what we experience as pain. Also, the influx of calcium ions via TRPA1 indirectly causes blood vessel dilation and tissue inflammation.
According to senior author Karel Talavera, the team's findings are an important step in developing a solution to treat such infections.
"The identification of TRPA1 as a molecular determinant of direct LPS effects on pain-sensing neurons offers new insights into the pathogenesis of pain and neurovascular responses during bacterial infections and opens novel avenues for their treatment," she said in a statement.
