Abstract

Objectives: 1)I Investigate the baseline histological characteristics of sinonasal tissue in wild-type mice. 2) Observe the effects of knocking out various genes involved in innate immunity on the inflammatory cell infiltrates and mucosal architecture of murine sinonasal epithelium. Methods: Unchallenged wild-type C57-BL6 mice, as well as knockouts for the innate immunity genes NOD-1, NOD-2, RIP-2, TLR-2 and MYD88, were sacrificed at age of maturity. The heads were decalcified and sinuses serially cut at 5 micrometer thickness. Three sections of the nasal cavity (anterior, mid, and posterior) were selected and examined under H&E and immunohistochemical staining conditions. Goblet cells, basement membrane thickness, neutrophil, macrophages, and eosinophils were evaluated and counted under high-power field and compared using one-way analysis of variance multiple comparison (SPSS 20). Results: Average cell counts per mm2 for wild-type mice were 16.3 +- 1.5 macrophages, 2.0 +- 0.5 neutrophils, 0 eosinophils, and 2152.4 +- 572.4 goblet cells; basement membrane thickness was 3.1 +- 1.5 micro meter. There were no significant differences between the wild-type and the knockout groups. Conclusions: The current study suggests that innate immunity gene knockouts had little effect on the sinonasal epithelium of unchallenged mice. Disruption of innate immune effector genes is not sufficient in and of itself to cause a rhinosinusitis phenotype in mice, but may still cause an inability to mount an appropriate host immune response to microbial pathogens.

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