The pathogenesis of canine sino-nasal aspergillosis (SNA) and lymphoplasmacytic rhinitis (LPR) remains poorly understood. The innate immune system is implicated in the etiology of human chronic rhinosinusitis. Therefore, we hypothesized that dysfunction in innate immunity could be implicated in the pathogenesis of SNA and LPR. Expression of messenger RNA (mRNA) encoding Toll-like receptors (TLRs) 1-10 and NOD-like receptors (NODs) 1 and 2 in nasal mucosal biopsies from SNA or LPR dogs was compared with mucosa from healthy controls. Gene expression was quantified using quantitative real-time reverse transcriptase polymerase chain reaction normalized against multiple housekeeper genes. All TLR and NOD genes were quantified in all samples. SNA was associated with significantly increased expression of TLRs 1-4, 6-10; and NOD2, relative to controls. LPR was associated with significantly increased expression of TLRs 1, 2, 6-8, relative to controls. There was significantly more expression of TLRs 1, 4, 6-10 and NOD2 in SNA dogs than in LPR dogs. The significance of these differences in the pathogenesis of these diseases is yet to be determined.
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