Differential expression of interleukin‐32 in chronic rhinosinusitis with and without nasal polyps

Abstract

Background Chronic rhinosinusitis (CRS) is a heterogeneous disease characterized by local inflammation of the upper airways and sinuses and is frequently divided into polypoid CRS (CRSwNP) and non-polypoid CRS (CRSsNP). However, the mechanism of inflammation in CRS has still not been fully elucidated. The aim of the study was to investigate the role of IL-32, a recently discovered proinflammatory cytokine, in CRS. Methods We collected nasal epithelial cells and nasal tissue from patients with CRS and control subjects. We assayed mRNA for IL-32 by real-time PCR and measured IL-32 protein by ELISA, western blot and immunohistochemistry. Results The expression of mRNA for IL-32 was elevated in epithelial cells from uncinate tissue from patients with CRSsNP compared to patients with CRSwNP (p<0.05), control subjects (p=0.06) or epithelial cells from nasal polyp tissue (p<0.05). Production of IL-32 was induced by IFN-γ, TNF and dsRNA in primary airway epithelial cells. In whole tissue extracts, the expression of IL-32 protein was significantly elevated in patients with CRSwNP compared to patients with CRSsNP and control subjects. Immunohistochemistry data showed that IL-32 was detected in mucosal epithelial cells and inflammatory cells in the lamina propria. Levels of IL-32 were correlated with levels of CD3 and macrophage mannose receptor in nasal polyp tissue. Immunofluorescence data showed IL-32 co-localization with CD3 positive T cells and CD68 positive macrophages in nasal polyps. Conclusion Overproduction of IL-32 may be involved in the pathogenesis of CRS, although the role of IL-32 in the inflammation in CRSsNP and CRSwNP may be different.

Increased interleukin-32 expression in chronic hepatitis B virus-infected liver

“…IL-32 plays an important role in innate and adaptive immune response, 17 and is involved in many inflammatory disorders, such as chronic rhinosinusitis. 7 Recently, it was reported that HBeAg induces the expression of IL-1b, granulocyte macrophage-colony stimulating factor (GM-CSF) and TNF-a in hepatocytes. 18 IL-1b or TNF-a increases the expression of IL-32 by human hepatoma cells.…”

“…7 A recent study 8 proved that IL-32 is an important cytokine involved in the inflammation of allergic rhinitis (AR). In that study, IL-32 expression is increased in the nasal mucosa of AR patients and the level of IL-32 expression in nasal mucosa tissue from AR patients correlates with inflammation, IL-1b, IL-18.…”

International Consensus Statement on Allergy and Rhinology: Rhinosinusitis

“…528 In addition to host defense molecules, ECs respond to PRR stimulation with the secretion of cytokines and chemokines that foster inflammation and attract and activate innate effector cells. 362,515,[529][530][531][532] In addition, the EC cytokines play a key role in shaping any subsequent adaptive immune response. Cytokine crosstalk between ECs, innate lymphoid cells (ILCs), and dendritic cells matches the appropriate innate and adaptive response to particular foreign stimuli.…”

Expression of Clara cell 10-kDa protein and trefoil factor family 1 in patients with chronic rhinosinusitis and nasal polyps

“…This has led to the classification of CRS as either CRS with nasal polyps (CRSwNP) or CRS without nasal polyps (CRSsNP) (4). It has been demonstrated that the pro-inflammatory cytokine interleukin-32, is differentially expressed in the nasal epithelial cells of patients with CRSwNP and those with CRSsNP (5). Although the differential expression of inflammatory mediators in CRSwNP and CRSsNP has been previously demonstrated (6), further studies are required to provide a basis for the accurate diagnosis and the development of effective treatment strategies.…”