Deletion of Reduces Eosinophilic Inflammation and Interleukin-5 Expression in a Murine Model of Rhinitis.

Background: ARF nucleotide-binding site opener (ARNO) is a guanine nucleotide-exchange factor for ADP-ribosylation factor proteins. ARF nucleotide-binding site opener also binds MyD88, and small-molecule inhibition of ARNO reduces inflammation in animal models of inflammatory arthritis and acute inflammation. However, whether genetic deletion of in mice reduces pathologic inflammation has not yet been reported. Furthermore, its role in the nasal cavity has yet to be investigated.

Objective: To generate knockout mice and to determine whether genetic loss of reduces eosinophilic inflammation in the ovalbumin (OVA) murine model of rhinitis.

Methods: knockout mice were generated and wild type and knockout littermates were subjected to the OVA-induced mouse model of rhinosinutitis. Eosinophilic inflammation was assessed through immunofluorescent quantification of EMBP eosinophils in the septal mucosa and cytokine expression was assessed by quantitative polymerase chain reaction.

Results: knockout mice are viable and fertile without any noted deficits. wild type and knockout mice subjected to the OVA-induced model of rhinitis demonstrated an average of 314.5 and 153.8 EMBP cells per mm septal tissue, respectively ( < .05). Goblet cells per mm of basal lamina were assessed via Alcian blue and there was no statistically significant difference between wild type and knockout mice. Ovalbumin-induced expression of interleukin-5 (IL-5) was significantly reduced in knockout mice ( < .05). There was no statistically significant reduction in IL-4, IL-13, or eotaxin-1 expression.

Conclusions: These data demonstrate that deletion of reduces eosinophilic inflammation and IL-5 expression in an OVA-induced model of rhinitis.