Bitter taste receptors in the upper airway were the first line of defense against sinus infections. However, the ability of the receptor to kill harmful toxins and pathogens was blocked when the sweet taste receptors were also triggered. An earlier study reported that glucose and other sugars triggered the sweet taste receptors. But the new study led by scientists at the Perelman School of Medicine of the University of Pennsylvania reported that amino acids could also trigger the sweet taste receptors. The new research could pave the way toward novel treatments for chronic sinus infections. The study findings were published in the journal Science Signaling.
Earlier Penn study had suggested that a new treatment for the infections involved manipulation of the nasal bitter and sweet taste receptors. Bitter receptors release small proteins (antimicrobial peptides) that destroy bacteria, viruses, and fungi which enter the nose, whereas sweet receptors control the release rate of the peptides. When the body was healthy, the system maintained the status quo. But when pathogens, toxins, and allergens entered the upper respiratory tract, the system throws off balance.
In the new research, scientists revealed that the sweet taste receptor (T1R) could also be activated by certain amino acids secreted by bacteria. The scientists took cells from rhinosinusitis patients and isolated the different groups of bacteria that were present. Staphylococcus bacterial cultures produced two D-amino acids called D-Phe and D-Leu, both of which activated T1R sweet receptors and blocked the antimicrobial peptides release, researchers reported.
The senior author of the study, Dr. Noam A. Cohen, director of rhinology research at Penn said, "These amino acids, which come from Staphylococcus bacteria, block the body's natural immune response by essentially hitting the breaks on the defensive, bitter taste receptors."
Also, the researchers showed the importance of sweet and bitter taste receptors in determining the microbial communities that exist in the human airway, which could also lead to specific therapies to treat chronic rhinosinusitis.
The study's lead author Robert Lee, Ph.D., an assistant professor of Otorhinolaryngology and Physiology at Penn said in the future, sweet-receptor blockers that used in some food and supplement products could be beneficial to block activation of T1R. Deactivation of T1R would let the body's normal defenses to work properly, although high concentrations of D-amino acids were present.