Staphylococcus aureus, Superantigens, and Nasal Polyps

Staphylococcus aureus (S. aureus) is associated with chronic rhinosinusitis with nasal polyps (CRSwNP), and may contribute to polyp formation through a variety of inflammatory mechanisms, biofilm formation, and epithelial barrier dysfunction. S. aureus enterotoxins act as superantigens resulting in excessive and uncoordinated immune responses in some nasal polyp patients. Superantigens directly activate T cells by binding MCH class II and T-cell receptor molecules and elicit an immune response independent of specific antigen recognition that evades antigen presenting cells. In addition to superantigen effects, S. aureus and related virulence factors induce a type 2 inflammatory response through polyclonal IgE production, immunoglobulin class switching, synergistic effects of fungal-induced inflammation, and altered eicosanoid metabolism. Furthermore, biofilms are a reservoir for bacteria, and are difficult to eliminate with antibiotic therapy, contributing to the persistence of S. aureus and downstream inflammation. Epithelial barrier dysfunction results from altered expression of tight junction proteins in the nasal mucosa in the presence of S. aureus, and ultimately is a contributing factor to polyp formation. Therapeutic targets directed on S. aureus and indirect on resulting inflammation have been described and continued to be investigated as part of the treatment of CRSwNP.