In order to access the sinus membrane, Aurora collaborated with assistant professor of otolaryngology at SLU Thomas Sanford, M.D. to collect samples from patients who were undergoing surgery. Thirty patients had chronic rhinosinusitus and 12 were healthy controls, undergoing surgery for other reasons.
Once the samples were gathered, researchers examined two particular microbe genes bacterial 16S and fungal 18S ribosomal RNA genes and analyzed them with deep sequencing techniques.
"It turned out that the CRS and control groups were very similar, and the differences were not of the type that that would cause disease," Aurora said. "It did not appear that a particular microorganism was acting as a pathogen."
"So, we turned to look at the immune system."
And, indeed, Aurora and his team found that the immune system of those with CRS was activated by the microbiota of healthy individuals.
Further study findings suggested that bacteria and fungi are not causing an infection in the sinuses, but rather, that the immune system was responding to commensals, microorganisms that, themselves, do not harm the human body. When the immune system reacts in a hyper-responsive way, unnecessarily fighting off a harmless microorganism, it can initiate an immune response like inflammation. The body can then get locked into a cycle where inflammation generates more inflammation, causing a chronic condition.
"Patients with CRS are hyper-responsive to normal microbiota," said Aurora. "Our take-home message is that the problem doesn't lie in the microbiota. The inflammatory response and the resulting damage from
|Contact: Carrie Bebermeyer|
Saint Louis University