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饮食诱导的肥胖会加重 Rag1 小鼠中 NK 细胞介导的接触性超敏反应。

Diet-induced obesity aggravates NK cell-mediated contact hypersensitivity reaction in Rag1 mice.

机构信息

Department of Medical Biology, Faculty of Health Sciences, Jagiellonian University Medical College, Krakow, Poland.

出版信息

Contact Dermatitis. 2021 Sep;85(3):307-316. doi: 10.1111/cod.13871. Epub 2021 May 11.

DOI:10.1111/cod.13871
PMID:33899952
Abstract

BACKGROUND

Previous studies showed that natural killer (NK) cells mediate contact hypersensitivity (CHS) reaction. Many reports are showing that obesity promotes several inflammatory diseases. It was shown that diet-induced obesity (DIO) aggravates classical T cell-mediated CHS in mice.

OBJECTIVES

To determine whether the high-fat diet (HFD)-induced obesity modulates antigen-specific NK cell-mediated response.

METHODS

We evaluated the effect of DIO on NK cell-mediated CHS reaction using a model of dinitrofluorobenzene (DNFB)-induced CHS in Rag1 mice.

RESULTS

Rag1 mice fed HFD for 8 but not for 4 weeks developed aggravated CHS reaction determined by ear swelling measurement when compared to animals kept on normal diet (ND) prior to DNFB sensitization. The obese Rag1 mice presented the adipose tissue inflammation. Furthermore, in vitro analysis showed that feeding with HFD significantly increases interferon γ (IFN-γ) and interleukin (IL)-12p70 and decreases adiponectin concentration in liver mononuclear cell (LMNC) culture supernatants. The flow cytometry analysis of LMNC revealed that HFD treatment prior to DNFB sensitization increases the percentage of NK1.1 IFN-γ cell population and affects the development and maturation of NK1.1 cells.

CONCLUSIONS

In summary, current results suggest that the DIO significantly modulates the local and systemic inflammatory response, contributing to exacerbation of the CHS response mediated by liver NK cells.

摘要

背景

先前的研究表明自然杀伤 (NK) 细胞介导接触性超敏反应 (CHS)。许多报告表明肥胖会促进多种炎症性疾病。有研究表明,饮食诱导的肥胖 (DIO) 会加重小鼠经典 T 细胞介导的 CHS。

目的

确定高脂肪饮食 (HFD) 诱导的肥胖是否会调节抗原特异性 NK 细胞介导的反应。

方法

我们使用二硝基氟苯 (DNFB) 诱导的 CHS 模型评估了 DIO 对 NK 细胞介导的 CHS 反应的影响,该模型在 Rag1 小鼠中进行。

结果

与在进行 DNFB 致敏之前一直食用正常饮食 (ND) 的动物相比,喂养 HFD 8 周而不是 4 周的 Rag1 小鼠通过耳朵肿胀测量确定发生了加重的 CHS 反应。肥胖的 Rag1 小鼠表现出脂肪组织炎症。此外,体外分析表明,用 HFD 喂养会显著增加肝脏单核细胞 (LMNC) 培养上清液中干扰素 γ (IFN-γ) 和白细胞介素 (IL)-12p70 的浓度,同时降低脂联素浓度。在进行 DNFB 致敏之前用 HFD 处理的 LMNC 的流式细胞术分析表明,增加了 NK1.1 IFN-γ 细胞群的百分比,并影响了 NK1.1 细胞的发育和成熟。

结论

总之,目前的结果表明,DIO 显著调节局部和全身炎症反应,导致肝脏 NK 细胞介导的 CHS 反应加剧。

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Contact Dermatitis. 2021 Sep;85(3):307-316. doi: 10.1111/cod.13871. Epub 2021 May 11.
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