IL‐32 up‐regulation is associated with inflammatory cytokine production in allergic rhinitis

Abstract

IL-32 is a described pro-inflammatory cytokine produced by T lymphocytes, natural killer cells, monocytes, and epithelial cells. However, the specific mechanism of IL-32 on allergic rhinitis (AR) has not been elucidated. Here, we report a significant increase of IL-32 protein and mRNA in the nasal mucosa of AR patients. In addition, in nasal mucosa tissue from AR patients, the level of IL-32 production correlated with inflammation, IL-1β, IL-18, and granulocyte-macrophage colony-stimulating factor (GM-CSF). In an AR animal model, IL-32 significantly increased IgE and inflammatory cytokine levels. IL-32 expression was induced by recombinant human GM-CSF via activation of caspase-1 in eosinophils. In addition, depletion of IL-32 prevents the production of inflammatory cytokines in eosinophils. In conclusion, IL-32 is an important cytokine involved in the inflammation of AR. The regulation of IL-32 expression may form the basis of a new strategy for the treatment of AR.

Inhibition of IL-32 and TSLP production through the attenuation of caspase-1 activation in an animal model of allergic rhinitis by Naju Jjok (Polygonum tinctorium)

“…The eosinophil granule proteins play a central role in the development of rhinitis (32). IL-32 released from eosinophils has been shown to significantly increase the levels of IgE and inflammatory cytokines, including IL-1β, IL-18 and GM-CSF in AR (7). Despite the absence of a Th1-cell predominant inflammation, other Th2-type inflammatory disorders, such as AR, asthma and AD have been linked with increased levels of IL-32 (33).…”

“…GM-CSF is an important activating factor for eosinophils and neutrophils, and is known as a pleiotropic and pro-inflammatory cytokine (6). GM-CSF induced the expression of IL-32 in eosinophils (7).…”

“…IL-32 is associated with AR, cancer, infection and chronic inflammation (7,(8)(9)(10). IL-32 is a cytokine produced mainly by immune cells, including T lymphocytes, natural killer cells, epithelial cells, mast cells, keratinocytes, eosinophils and blood monocytes (11,12).…”

“…IL-32 is a cytokine produced mainly by immune cells, including T lymphocytes, natural killer cells, epithelial cells, mast cells, keratinocytes, eosinophils and blood monocytes (11,12). IL-32 has previously been shown to contribute to pro-inflammatory cytokine synthesis (7). Several pathways have been shown to be involved in inflammatory processes, including the phosphatidylinositide 3-kinase (PI3K)/Akt pathway, nuclear factor (NF)-κB/AP-1 pathway, p38 mitogen-activated protein kinase (MAPK) and caspase-1 pathways (7,12,13).…”

“…IL-32 has previously been shown to contribute to pro-inflammatory cytokine synthesis (7). Several pathways have been shown to be involved in inflammatory processes, including the phosphatidylinositide 3-kinase (PI3K)/Akt pathway, nuclear factor (NF)-κB/AP-1 pathway, p38 mitogen-activated protein kinase (MAPK) and caspase-1 pathways (7,12,13). Viral-induced IL-32 expression seems to be mediated by cyclooxygenase-2 (COX-2) pathways (14).…”