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首页> 外文期刊>Biology Open >IL-31 plays dual roles in lung inflammation in an OVA-induced murine asthma model
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IL-31 plays dual roles in lung inflammation in an OVA-induced murine asthma model

机译：IL-31在OVA诱导的小鼠哮喘模型中在肺部炎症中起双重作用

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Interleukin 31 (IL-31) is a four-helix cytokine made predominantly by Th2 CD4+T cells. It was initially identified as being associated with the promotion of atopic dermatitis, where increased levels of IL-31 levels have been found and IL-31 induced the expression of proinflammatory cytokines and chemokines in a human bronchial epithelial cell line. However, subsequent study has shown that IL-31RA knockout mice developed exacerbated type 2 inflammation in the lung following infection withSchistosoma mansonieggs. In this study, we investigated the dynamic expression of IL-31 and IL-31RA during eight consecutive ovalbumin (OVA) challenges and measured the chemokines from lung alveolar epithelial cells induced by IL-31. In addition, we examined the effect deletion of IL-31RA has on lung inflammation and the differentiation of CD4+T cells. Our results demonstrate that the expression of IL-31 and IL-31RA was elevated after each weekly OVA challenge, although slightly less of both observed after the first week of OVA challenge. IL-31 also promoted the expression of inflammatory chemokines CCL5, CCL6, CCL11, CCL16, CCL22, CCL28, CX3CL1, CXCL3, CXCL14 and CXCL16 in alveolar epithelial cells. Migration of macrophages and T cells was enhanced by culture supernatants of IL-31-stimulated alveolar epithelial cells. Lastly, and in contrast to the IL-31 results, mice deficient in IL-31RA developed exacerbated lung inflammation, increased IL-4-positive cell infiltrates and elevated Th2 cytokine responses in draining lymph nodes. The proliferation of IL-31RA?/?CD4+T cells was enhancedin vitroafter anti-CD3/anti-CD28 antibody stimulation. These data indicate that IL-31/IL-31RA may play dual roles, first as an early inflammatory mediator promoting the secretion of chemokines to recruit inflammatory cells, and subsequently as a late inflammatory suppressor, limiting Th2 cytokine responses in allergic asthma.
机译：白介素31（IL-31）是一种主要由Th2 CD4 + T细胞制造的四螺旋细胞因子。最初被鉴定为与特应性皮炎的促进有关，其中已发现IL-31水平升高，IL-31诱导人支气管上皮细胞系中促炎细胞因子和趋化因子的表达。然而，随后的研究表明，IL-31RA基因敲除小鼠在感染曼氏血吸虫后，在肺部加剧了2型炎症。在这项研究中，我们调查了八个连续的卵清蛋白（OVA）攻击过程中IL-31和IL-31RA的动态表达，并测量了IL-31诱导的肺泡上皮细胞的趋化因子。此外，我们检查了IL-31RA缺失对肺部炎症和CD4 + T细胞分化的影响。我们的结果表明，在每周一次OVA攻击后，IL-31和IL-31RA的表达均升高，尽管在OVA攻击的第一周后两者均略低。 IL-31还促进了肺泡上皮细胞中炎症趋化因子CCL5，CCL6，CCL11，CCL16，CCL22，CCL28，CX3CL1，CXCL3，CXCL14和CXCL16的表达。 IL-31刺激的肺泡上皮细胞的培养上清液可增强巨噬细胞和T细胞的迁移。最后，与IL-31结果相反，缺乏IL-31RA的小鼠在引流淋巴结中发展为加剧的肺部炎症，IL-4阳性细胞浸润增加和Th2细胞因子应答升高。抗CD3 /抗CD28抗体刺激后，IL-31RAα/βCD4+ T细胞的增殖在体外得以增强。这些数据表明，IL-31 / IL-31RA可能起双重作用，首先作为促进趋化因子分泌以募集炎症细胞的早期炎症介质，然后作为晚期炎症抑制剂抑制了过敏性哮喘中Th2细胞因子的反应。

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