Patients with chronic rhinosinusitis (CRS) in general, and those with nasal polyps (CRSwNP) in particular, have been shown to have down-regulation of tight junction genes. Zinc, on the other hand, is well-known for its role in immune regulation and deficiency has been suggested to induce barrier dysfunction in disorders such as inflammatory bowel diseases. Zinc haemostasis in CRS and its effects on barrier dysfunction in the nose are still unclear. These authors utilised a microarray of tissue cores obtained from 35 patients: 28 CRS, of which 19 with nasal polyps and seven controls. Specimens were stained with anti-ZO-1 antibodies and the zinc fluorophore Zinquin. Additionally, human nasal epithelial cell air-liquid interface cultures were grown in zinc deplete media for two weeks. The results showed that Zinc levels were significantly less than controls in the nasal epithelium of CRS patients with nasal polyps. It was also noted that in a zinc-deficient medium, there was significant reduction in transepithelial electrical resistance with increased paracellular permeability. The authors concluded that zinc homeostasis is altered in CRSwNP and intramucosal zinc depletion negatively affects mucosal barrier structure and function. This is an interesting article showing that there are still multiple targets for medical therapy in CRS patients and research in other chronic inflammatory conditions could be studied in CRS patients.

Mucosal zinc deficiency in chronic rhinosinusitis with nasal polyposis contributes to barrier disruption and decreases ZO-1.
J. Murphy, M. Ramezanpour, E. Roscioli, et al.
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Hassan Mohammed

North East Deanery, Newcastle, UK.

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