Inflammasome gene expression alterations in Staphylococcus aureus biofilm-associated chronic rhinosinusitis

Background: The role of inflammasomes in chronic inflammation has been the subject of intense research in recent years. Chronic rhinosinusitis (CRS), a persistent inflammatory disease, continues to be investigated hoping that a clearer pathophysiologic description will guide discovery of future treatment modalities. This study investigates the role of inflammasome complexes in CRS patients with Staphylococcus aureus biolm infection, a key culprit associated with disease severity and recalcitrance. Methodology: Sinonasal tissue samples were collected from CRS patients with (P+) and without (P-) polyps and controls. S. aureus biolm status was obtained using fluorescence in situ hybridization and classied as biolm positive (B+) or negative (B-). RNA was analysed using a Human Inflammasome PCR array, proling the expression of 84 genes involved in inflammasome function. Results: Sixteen samples were obtained: 5 B+P+, 5 B-P-and 6 controls. Comparing B+P+ vs. controls showed the greatest number of differentially expressed genes. In particular, Absent in Melanoma 2 (AIM2) was consistently and signicantly up-regulated in the B+P+ vs. B-P-and controls. In contrast, when comparing the B-P-vs. controls, no genes showed signicant changes. Conclusion: Our results indicate the involvement of inflammasome complexes and their signalling pathways in CRS patients with polyps and S. aureus biolms. In particular, AIM2, activated by intracellular double-stranded DNA, is up-regulated in this group, implying that S. aureus may play a role in intracellular triggering of the inflammasome response. Studies with further patient stratification and assessing corresponding protein expression are needed to further characterize the role of inflammasomes in CRS.