Interleukin-9 and interleukin-17C in chronic rhinosinusitis.

Abstract

Interleukin (IL)-9 and IL-17C have been known to play a role in allergic inflammation, yet, their roles in chronic rhinosinusitis (CRS) are not well defined. IL-9 induces changes in epithelial cell gene expression leading to goblet cell metaplasia, whereas IL-17C is functionally distinct in that its expression can be induced by bacterial challenge and inflammatory stimuli. This study aimed to compare levels of IL-9 and IL-17C in CRS with nasal polyps (CRSwNP) and without nasal polyps (CRSsNP) as well as atopy. Nasal polyp or sinus mucosal specimens from CRSwNP (n = 36), CRSsNP (n = 9), and control (n = 9) groups were collected and processed. Patient atopy status was determined by history of skin-prick test and pulmonary function test. Immunohistochemistry was carried out using anti-human IL-9 and IL-17C antibodies. Positively-stained cells were enumerated under high-power (×400) magnification in 5 consecutive fields. The level of expression of IL-9 was higher in CRSwNP than CRSsNP and control. Similar findings were demonstrated in IL-17C with higher expression in CRSwNP than CRSsNP and control. Both the averages of positively-stained cells expressing IL-9 and IL-17C were higher in CRS with asthma and allergy compared to control. This suggested that IL-9 and IL-17C were both involved in the pathogenesis of CRS, allergy, and asthma. Inflammatory cell expression of IL-9 and IL-17C were increased in CRS, particularly with allergy and asthma. These interleukins may contribute to the pathogenesis of CRSwNP as well as atopy and may serve as therapeutic targets for disease management.