Heather L Caslin, W Reid Bolus, Christopher Thomas, Shinji Toki, Allison E Norlander, R Stokes Peebles, Alyssa H Hasty
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Interestingly, BSA elicited epithelial IL-33 production, as well as gene expression for type 2 cytokines and IgE production that were dependent on IL-33. Moreover, multiple models of OVA sensitization also drove AT eosinophilia. Following transplantation of a donor fat pad with BSA-induced eosinophilia, OVA-sensitized recipient mice had higher numbers of bronchoalveolar lavage eosinophils that were recipient derived. Interestingly, lungs of recipient mice contained eosinophils, macrophages, and CD8 T cells from the donor AT. These trafficked similarly from BSA- and non-BSA-treated AT, suggesting even otherwise healthy AT serves as a reservoir of immune cells capable of migrating to the lungs. In conclusion, our studies suggest that i.p. injections of BSA and OVA induce an allergic response in the AT that elicits eosinophil recruitment, which may be an important consideration for those using OVA in animal models of allergic disease.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10759155/pdf/","citationCount":"0","resultStr":"{\"title\":\"Bovine Serum Albumin Elicits IL-33-Dependent Adipose Tissue Eosinophilia: Potential Relevance to Ovalbumin-induced Models of Allergic Disease.\",\"authors\":\"Heather L Caslin, W Reid Bolus, Christopher Thomas, Shinji Toki, Allison E Norlander, R Stokes Peebles, Alyssa H Hasty\",\"doi\":\"10.4049/immunohorizons.2300061\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>All cells of the immune system reside in adipose tissue (AT), and increasing type 2 immune cells may be a therapeutic strategy to improve metabolic health. In our previous study using i.p. IL-5 injections to increase eosinophils, we observed that a standard vehicle control of 0.1% BSA also elicited profound AT eosinophilia. In this study, we aimed to determine whether BSA-induced AT eosinophilia results in metabolic benefits in murine models of diet-induced obesity. I.p. 0.1% BSA injections increased AT eosinophils after 4 wk. Despite elevating eosinophils to >50% of immune cells in the AT, body weight and glucose tolerance were not different between groups. Interestingly, BSA elicited epithelial IL-33 production, as well as gene expression for type 2 cytokines and IgE production that were dependent on IL-33. Moreover, multiple models of OVA sensitization also drove AT eosinophilia. Following transplantation of a donor fat pad with BSA-induced eosinophilia, OVA-sensitized recipient mice had higher numbers of bronchoalveolar lavage eosinophils that were recipient derived. Interestingly, lungs of recipient mice contained eosinophils, macrophages, and CD8 T cells from the donor AT. These trafficked similarly from BSA- and non-BSA-treated AT, suggesting even otherwise healthy AT serves as a reservoir of immune cells capable of migrating to the lungs. 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引用次数: 0
摘要
免疫系统的所有细胞都驻留在脂肪组织(AT)中,增加2型免疫细胞可能是改善代谢健康的一种治疗策略。在我们之前利用静脉注射 IL-5 来增加嗜酸性粒细胞的研究中,我们观察到 0.1% BSA 的标准载体对照也会引起严重的 AT 嗜酸性粒细胞增多。在这项研究中,我们旨在确定 BSA 诱导的 AT 嗜酸性粒细胞增多是否会在饮食诱发肥胖的小鼠模型中产生代谢益处。静脉注射 0.1% BSA 会在 4 周后增加嗜酸性粒细胞。尽管嗜酸性粒细胞在胃肠道免疫细胞中所占比例升高到了 50%以上,但体重和糖耐量在不同组间并无差异。有趣的是,BSA 可诱导上皮细胞 IL-33 的产生,以及依赖于 IL-33 的 2 型细胞因子和 IgE 产生的基因表达。此外,多种 OVA 致敏模型也会引起 AT 嗜酸性粒细胞增多。在移植了由 BSA 诱导的嗜酸性粒细胞增多的供体脂肪垫后,OVA 致敏的受体小鼠支气管肺泡灌洗液中嗜酸性粒细胞的数量更高,而这些嗜酸性粒细胞是受体衍生的。有趣的是,受体小鼠的肺中含有来自供体 AT 的嗜酸性粒细胞、巨噬细胞和 CD8 T 细胞。这些细胞从经 BSA 处理和未经 BSA 处理的肺动脉瓣中迁移的情况相似,这表明即使是健康的肺动脉瓣也是一个能够迁移到肺部的免疫细胞库。总之,我们的研究表明,静注 BSA 和 OVA 会诱导 AT 产生过敏反应,从而引起嗜酸性粒细胞的募集,这可能是过敏性疾病动物模型中使用 OVA 的一个重要考虑因素。
Bovine Serum Albumin Elicits IL-33-Dependent Adipose Tissue Eosinophilia: Potential Relevance to Ovalbumin-induced Models of Allergic Disease.
All cells of the immune system reside in adipose tissue (AT), and increasing type 2 immune cells may be a therapeutic strategy to improve metabolic health. In our previous study using i.p. IL-5 injections to increase eosinophils, we observed that a standard vehicle control of 0.1% BSA also elicited profound AT eosinophilia. In this study, we aimed to determine whether BSA-induced AT eosinophilia results in metabolic benefits in murine models of diet-induced obesity. I.p. 0.1% BSA injections increased AT eosinophils after 4 wk. Despite elevating eosinophils to >50% of immune cells in the AT, body weight and glucose tolerance were not different between groups. Interestingly, BSA elicited epithelial IL-33 production, as well as gene expression for type 2 cytokines and IgE production that were dependent on IL-33. Moreover, multiple models of OVA sensitization also drove AT eosinophilia. Following transplantation of a donor fat pad with BSA-induced eosinophilia, OVA-sensitized recipient mice had higher numbers of bronchoalveolar lavage eosinophils that were recipient derived. Interestingly, lungs of recipient mice contained eosinophils, macrophages, and CD8 T cells from the donor AT. These trafficked similarly from BSA- and non-BSA-treated AT, suggesting even otherwise healthy AT serves as a reservoir of immune cells capable of migrating to the lungs. In conclusion, our studies suggest that i.p. injections of BSA and OVA induce an allergic response in the AT that elicits eosinophil recruitment, which may be an important consideration for those using OVA in animal models of allergic disease.