Polymeric immunoglobulin receptor and immunoglobulin A system in an eosinophilic mouse model of chronic rhinosinusitis

Abstract

Background: Chronic rhinosinusitis (CRS) is an inflammatory respiratory disease with symptoms of nasal blockade, headache, loss of smell and nasal secretions. It affects 11% of european population and is a global health burden. CRS is classified according to inflammatory profile as Type 2 eosinophilic or non-Type 2 neutrophilic CRS. Currently, the pathogenesis of CRS is not fully understood. Patients with selective IgA-deficiency present more often with CRS and an observational study showed a decreased polymeric immunoglobulin receptor (pIgR) expression and specific IgA response towards relevant antigens, such as Staphylococcus aureus enterotoxin B (SEB).

Aims: We aimed at elucidating the role of the pIgR/IgA pathway by using a mouse model of Type 2 CRS.

Methods: Type 2 CRS mouse model was established by intranasal ovalbumin (OVA) and SEB instillations after i.p. sensitization to OVA. Inflammatory and IgA-related parameters were evaluated on decalcified skulls by means of histology and on serum and nasal lavage by means of ELISA. To test the role of pIgR, we repeated the model in pIgR^−/−mice.

Results: Mice with experimental Type 2 CRS showed a significant increase in epithelial thickness, sinus fibrosis, eosinophilic infiltration and IgA levels in nasal lavage compared to controls. Also, a significant increase was seen in IgA and pIgR sinus tissue expression. However, no significant changes were seen in inflammatory markers between pIgR^−/− mice and WT controls.

Conclusion: Type 2 CRS is linked to an increased sinonasal pIgR expression with increased IgA production and release in an in vivo mouse model. Lack of pIgR does not seem to affect the induction of Type 2 CRS.