2014•BMC ImmunologyOpen access

Exogenous interleukin-10 alleviates allergic inflammation but inhibits local interleukin-10 expression in a mouse allergic rhinitis model

Shui-Bin Wang, Yuqin Deng, Jie Ren, Bokui Xiao, Zheng Liu, Zezhang Tao

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Abstract

BACKGROUND: Interleukin-10 (IL-10) has an important anti-inflammatory and immunoregulatory function, and its expression is negatively correlated with the development and severity of allergic rhinitis (AR). However, the in vivo effects of exogenous IL-10 on AR have not been studied and the mechanisms underlying the effects of IL-10 have not been fully understood. Here, we investigated the effects of intranasal administration of recombinant mouse (rm) IL-10 on the expression of Th responses and local IL-10 in a mouse model of AR induced by ovalbumin. RESULTS: Administration of rmIL-10 during challenge significantly reduced the number of eosinophils and mast cells, as well as Type 2 helper T (Th2) and Th17 cell related cytokine and transcription factor levels in the nasal mucosa and nasal lavage fluid in AR mice. The rmIL-10 treatment significantly inhibited the number of IL-10-positive cells and IL-10 mRNA expression in the nasal mucosa in AR mice. CONCLUSION: Our results show that exogenous IL-10 administrated in challenge phase alleviates nasal allergic inflammation in AR mice, most likely by inhibiting Th2 and Th17 responses. It can also inhibit local IL-10 levels in the nasal mucosa. Our findings indicate that IL-10 may have the potential as an inhibitor of AR.

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BACKGROUND: Interleukin-10 (IL-10) has an important anti-inflammatory and immunoregulatory function, and its expression is negatively correlated with the development and severity of allergic rhinitis (AR). However, the in vivo effects of exogenous IL-10 on AR have not been studied and the mechanisms underlying the effects of IL-10 have not been fully understood. Here, we investigated the effects of intranasal administration of recombinant mouse (rm) IL-10 on the expression of Th responses and local IL-10 in a mouse model of AR induced by ovalbumin. RESULTS: Administration of rmIL-10 during challenge significantly reduced the number of eosinophils and mast cells, as well as Type 2 helper T (Th2) and Th17 cell related cytokine and transcription factor levels in the nasal mucosa and nasal lavage fluid in AR mice. The rmIL-10 treatment significantly inhibited the number of IL-10-positive cells and IL-10 mRNA expression in the nasal mucosa in AR mice. CONCLUSION: Our results show that exogenous IL-10 administrated in challenge phase alleviates nasal allergic inflammation in AR mice, most likely by inhibiting Th2 and Th17 responses. It can also inhibit local IL-10 levels in the nasal mucosa. Our findings indicate that IL-10 may have the potential as an inhibitor of AR.

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Available abstract

BACKGROUND: Interleukin-10 (IL-10) has an important anti-inflammatory and immunoregulatory function, and its expression is negatively correlated with the development and severity of allergic rhinitis (AR). However, the in vivo effects of exogenous IL-10 on AR have not been studied and the mechanisms underlying the effects of IL-10 have not been fully understood. Here, we investigated the effects of intranasal administration of recombinant mouse (rm) IL-10 on the expression of Th responses and local IL-10 in a mouse model of AR induced by ovalbumin. RESULTS: Administration of rmIL-10 during challenge significantly reduced the number of eosinophils and mast cells, as well as Type 2 helper T (Th2) and Th17 cell related cytokine and transcription factor levels in the nasal mucosa and nasal lavage fluid in AR mice. The rmIL-10 treatment significantly inhibited the number of IL-10-positive cells and IL-10 mRNA expression in the nasal mucosa in AR mice. CONCLUSION: Our results show that exogenous IL-10 administrated in challenge phase alleviates nasal allergic inflammation in AR mice, most likely by inhibiting Th2 and Th17 responses. It can also inhibit local IL-10 levels in the nasal mucosa. Our findings indicate that IL-10 may have the potential as an inhibitor of AR.

Key concepts: Mucous membrane of nose, Ovalbumin, Allergic inflammation, Immunology, Inflammation, Nasal administration, Cytokine, Interleukin

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