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Comparison of Inflammatory Changes in Ethmoid Mucosa and Nasal Turbinate Tissue: A Histopathological Study

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Abstract:
Background: Chronic rhinosinusitis (CRS) is defined as symptomatic inflammation of the nose and paranasal sinuses lasting more than 12 weeks. Persistent inflammation is thought to originate from multiple factors

Abstract:
Background: Chronic rhinosinusitis (CRS) is defined as symptomatic inflammation of the nose and paranasal sinuses lasting more than 12 weeks. Persistent inflammation is thought to originate from multiple factors including host physical and innate barrier defects and the exposure of the sinonasal mucosa to exogenous microorganisms. Regional differences in the innate host defense molecules present in nasal and sinus tissue have been recently reported. Thus, a histopathological study was conducted by Lal et al. to compare inflammatory changes in the ethmoid sinus mucosa and nasal turbinate tissue for CRS patients and controls. The objective of this work was to interpret the histopathological data from an immunobiological perspective and describe the significance of the results within the context of current scientific literature.
Methods: Tissue samples were collected from sinonasal surgery patients in three specific regions: ethmoid cells ± uncinate process (EC) in all patients and the inferior (IT) or middle turbinate (MT). EC and IT/MT samples were compared using Cohen’s kappa coefficient to measure agreement based on overall severity of inflammation, eosinophil count per high power field, and the predominant inflammatory cell infiltrate. The results of this study were compared with the current cohort of scientific literature regarding CRS pathogenesis. Both previous and current hypotheses were considered to construct a holistic overview of the development of the current understanding of CRS.
Results: The histopathology study determined that regional differences in degree and type of inflammation may be present in the nose and paranasal cavity. These findings support the current understanding of CRS as an inflammatory disease that is likely mediated by both host and environmental factors.
Conclusions: The histopathology study supports the current cohort of CRS research and provides evidence in support of the involvement of host factors in CRS pathogenesis.

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Date Created
  • 2017-05

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Effects of Surfactant Protein-A on the Production of Mucin5AC in the Sinonasal Epithelia of a Humanized Transgenic Mouse Model

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The Surfactant Protein-A family of proteins have long been observed to allocate immune responses in the lungs, although recent evidence has surfaced which suggests similar mechanisms involving these proteins may

The Surfactant Protein-A family of proteins have long been observed to allocate immune responses in the lungs, although recent evidence has surfaced which suggests similar mechanisms involving these proteins may occur in the sinonasal epithelia. In this study, the regulatory effects of SP-A on the production of Mucin5AC (mucus) in the sinuses of wild-type (control) and endogenous SP-A knock-out mice were investigated. The effects of human transgenic SP-A knock-in polymorphisms 223Gln (“risk” allele) and 223Lys (“non-risk” allele) on Mucin5AC production were also examined. It was theorized that SP-A optimally regulates Mucin5AC production and thereby some degree of innate immunity. Through inhibition of the SP-A gene, it was hypothesized that an increase in mucosal response would be observed in the endogenous SP-A knock-out samples. Upon examination, these in vivo samples consistently showed an increase in Mucin5AC production upon challenge with Pseudomonas aeruginosa strain K when compared to wild-type sets of the same treatment. The upregulation observed in the knock-out samples likely represented an ineffective mucosal response to unchecked bacterial replication in the absence of lipopolysaccharide-competitive SP-A aggregates. Mucin5AC upregulation was also observed in the 223Lys (“non-risk” allele) samples, although expression directed by this allelic variant is considered to characterize a healthy response to bacterial aggression, as the recognition/binding site on the carbohydrate domain of this polymorphism allows the effective aggregation of SP-A, which thereby promotes primary immune response in infected sinonasal tissue. Further studies will elucidate the specific molecular pathways leading to inflammatory and immune responses in the sinonasal epithelia, research which might, in the future, permit the development of novel diagnostic and therapeutic strategies in the clinical setting.

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Date Created
  • 2020-05