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Interleukin (IL)‐31 induces pro‐inflammatory cytokines in human monocytes and macrophages following stimulation with staphylococcal exotoxins
Author(s) -
Kasraie S.,
Niebuhr M.,
Werfel T.
Publication year - 2010
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2009.02255.x
Subject(s) - immunology , cytokine , stimulation , proinflammatory cytokine , monocyte , interleukin 10 , interleukin , secretion , receptor , cd86 , biology , medicine , immune system , inflammation , t cell , endocrinology
To cite this article: Kasraie S, Niebuhr M, Werfel T. Interleukin (IL)‐31 induces pro‐inflammatory cytokines in human monocytes and macrophages following stimulation with staphylococcal exotoxins. Allergy 2010; 65 : 712–721. Abstract Background: IL‐31 is a cytokine expressed by T cells following activation with cytokines or staphylococcal exotoxins. A major function of IL‐31 in atopic dermatitis (AD) is the induction of pruritus in the skin via the IL‐31 receptor on sensory nerve cells. However, the regulation of the IL‐31 receptor and pro‐inflammatory functions of IL‐31 in human monocytes and monocyte‐derived cells are yet to be studied in detail. Objective: To investigate the regulation and function of IL‐31 receptors in resting and activated human monocytes, macrophages and dendritic cells. Methods: Human monocytes, macrophages and dendritic cells were stimulated with staphylococcal exotoxins (SEB, α‐toxin) or cytokines (IFN‐γ, IL‐13). IL‐31RA expression and regulation were then investigated at both the mRNA and the protein level. Subsequently, functional effects of IL‐31 stimulation on cytokine secretion were measured at the protein level. Results: Staphylococcal exotoxins significantly up‐regulated IL‐31RA expression on monocytes and macrophages but not on dendritic cells at both the mRNA and the protein level. IL‐31 enhanced the secretion of IL‐1β, IL‐6 and IL‐18 and up‐regulated CD86 expression. In patients with AD, functional IL‐31RA was also detected following stimulation of PBMC with IFN‐γ. However, this was not observed in healthy individuals. Conclusion: IL‐31 induces pro‐inflammatory effects in activated human monocytes and macrophages. This may have implications for cutaneous inflammation in eczema where an over‐expression of IL‐31 has been described previously. Moreover, our findings provide a new link between staphylococcal colonization and the worsening of inflammation via IL‐31. Further therapeutic considerations may include IL‐31 as a target in AD.