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Abstract
BackgroundThe proinflammatory cytokine interleukin (IL)-17A is associated with eosinophil infiltration into the nasal mucosa in a mouse model of ovalbumin-induced allergic rhinitis. Chemotaxis of eosinophils is mediated primarily through C-C chemokine receptor type 3 (CCR3). However, the mechanism underlying the IL-17A-mediated enhancement of eosinophil recruitment via chemoattractants/chemokines remains unknown.ObjectivesIn this study, we assessed the contribution of IL-17A to eosinophil-related inflammation via the CCL7/CCR3 pathway in experimental allergic rhinitis.MethodsIL-17A knockout (KO) and wild-type (WT) BALB/c mice were injected intraperitoneally and challenged intranasally with OVA to induce allergic rhinitis. Various parameters of the allergic response were evaluated, and mRNA and protein levels of CCL7 and CCR3 in nasal tissue and serum were compared between the two groups. The chemotactic response to CCL7 with or without IL-17A in bone marrow-derived eosinophils (bmEos) from BALB/c mice was measured.ResultsIn the allergic rhinitis model, IL-17A deficiency significantly decreased nasal symptoms, serum IgE levels, and eosinophil recruitment to the nasal mucosa. CCL7 and CCR3 mRNA and protein levels were decreased in the nasal mucosa of IL-17A KO mice compared with the WT mice. BmEos showed a significantly increased chemotactic response to -low concentration of CCL7 in the presence of IL-17A compared with its absence.ConclusionThe suppression of nasal inflammation due of IL-17A deficiency in allergic rhinitis is partly responsible for the regulation of CCL7 secretion and eosinophil infiltration, which may be regulated via the CCL7/CCR3 pathway.
Highlights
Allergic rhinitis is a typical Th2 cytokine-dominant disease that involves the influx of numerous inflammatory cells, such as eosinophils and mast cells, into the nasal mucosa as well as elevated immunoglobulin E (IgE) production [1, 2]
Chemokine ligand 7 (CCL7) and chemokine receptor type 3 (CCR3) mRNA and protein levels were decreased in the nasal mucosa of IL-17A KO mice compared with the WT mice
Bone marrow-derived eosinophils (BmEos) showed a significantly increased chemotactic response to -low concentration of CCL7 in the presence of IL-17A compared with its absence
Summary
Allergic rhinitis is a typical Th2 cytokine-dominant disease that involves the influx of numerous inflammatory cells, such as eosinophils and mast cells, into the nasal mucosa as well as elevated immunoglobulin E (IgE) production [1, 2]. Few studies have examined the involvement of IL-17A in eosinophil infiltration at sites of inflammation. Th17 cells enhance eosinophilic airway inflammation, which is mediated by Th2 cells [6]. The proinflammatory cytokine interleukin (IL)-17A is associated with eosinophil infiltration into the nasal mucosa in a mouse model of ovalbumin-induced allergic rhinitis. Chemotaxis of eosinophils is mediated primarily through C-C chemokine receptor type 3 (CCR3). The mechanism underlying the IL-17A-mediated enhancement of eosinophil recruitment via chemoattractants/chemokines remains unknown
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