The pathophysiology of CRS is still unknown due to the multifactorial etiologies involved. Bacteria play a role in CRS’s pathogenesis through biofilm adhesion, intracellular persistence, or inducing inflammation secondary to toxins.

Researchers did this study to evaluate an experimental model of eosinophilic CRS using prolonged exposure to bacterial toxins.

After induction with OVA sensitization with a subcutaneous injection for two weeks, rabbits underwent surgery to insert an indwelling catheter into the maxillary sinus. The sinus was irrigated with OVA 3 times weekly for two weeks, followed by sinus irrigation with a bacterial toxin three times weekly for four weeks.

Sinuses exposed to bacterial toxins (SEB, LPS, and LTA) produced significant mucosal thickening with inflammatory cells’ infiltration, notably eosinophils. SEB was the only toxin that promoted a mixed pattern of inflammation, including eosinophilic and neutrophilic infiltration.

The model in the present study produced significant mucosal thickening and inflammation in the sinuses exposed to bacterial toxins, with histological changes analogous to what is observed in patients with CRS with nasal polyps. This model may serve as a basis for future investigation of eosinophilic CRS’s pathogenesis concerning bacterial toxins or as a model for testing new therapeutic modalities for this disease.