Selenium (Se) is an essential trace element found in the body. Se deficiency and M1/M2 imbalance are closely related to inflammation. Heat stress can decrease immune function and cause inflammation. In order to investigate whether Se deficiency can aggravate pneumonia caused by heat stress and the role of M1/M2 imbalance in the occurrence of pneumonia, 100 AA broilers were divided into two groups and fed the conventional diet (0.2 mg/kg Se) and the Se-deficient diet (0.03 mg/kg Se). After 40 days of feeding, the normal feeding group was randomly divided into a control group and a heat stress group. At the same time, the Se-deficient diet feeding group was randomly divided into a low Se group and a low Se heat stress group, with 25 chickens in each group. The model was established by exposure at 40℃. Six hours later, broilers were euthanized, and their lung tissues were collected. Hematoxylin and eosin staining, immunofluorescence, quantitative real-time PCR, and western blotting were used to detect lung histopathological changes and the expression of M1/M2 markers, nuclear receptor-κB (NF-κB) pathway genes, and heat shock proteins. Meanwhile, the activity and content of oxidative stress-related indices were also detected. We found that the expression of interleukin-1β, interleukin-6, interleukin-12, and tumor necrosis factor-α was upregulated and the expression of interleukin-2, interleukin-10, and interferon-γ was downregulated. Immunofluorescence showed that the expression of CD16 was increased, the expression of CD163 was weakened, and the M1/M2 imbalance was present. In addition, the NF-κB pathway was activated by the increased expressions of heat shock proteins and oxidative stress. There was an increase in malondialdehyde, nitric oxide, and inducible nitric oxide synthase content, while the activity of total antioxidant capacity, glutathione peroxidase, catalase, and superoxide dismutase decreased, and the expression of NF-κB and cyclooxygenase-2 increased. These results suggest that low Se induces M1/M2 imbalance through oxidative stress activation of the NF-κB pathway and aggravates lung tissue inflammation caused by heat stress. This study offers a theoretical basis for exploring the pathogenesis of various kinds of inflammation induced by Se deficiency from the perspective of M1/M2 and provides a reference for the prevention of such diseases.

中文翻译：

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硒缺乏通过破坏 M1/M2 平衡加剧了鸡的热应激性肺炎。

硒 (Se) 是人体必需的微量元素。硒缺乏和M1/M2失衡与炎症密切相关。热应激会降低免疫功能并引起炎症。为了研究硒缺乏是否会加重热应激引起的肺炎以及M1/M2失衡在肺炎发生中的作用，将100只AA肉鸡分为两组，分别饲喂常规日粮（0.2 mg/kg Se）和缺硒饮食（0.03 mg/kg Se）。喂养40天后，正常喂养组随机分为对照组和热应激组。同时，将缺硒日粮饲喂组随机分为低硒组和低硒热应激组，每组25只鸡。40℃曝光建立模型。六小时后，肉鸡被安乐死，并收集他们的肺组织。苏木精和伊红染色、免疫荧光、定量实时 PCR 和蛋白质印迹用于检测肺组织病理学变化和 M1/M2 标志物、核受体-κB (NF-κB) 通路基因和热休克蛋白的表达。同时，还检测了氧化应激相关指标的活性和含量。我们发现白细胞介素1β、白细胞介素6、白细胞介素12和肿瘤坏死因子-α的表达上调，白细胞介素2、白细胞介素10和干扰素-γ的表达下调。免疫荧光显示CD16表达升高，CD163表达减弱，存在M1/M2失衡。此外，热休克蛋白和氧化应激的表达增加激活了 NF-κB 通路。丙二醛、一氧化氮、诱导型一氧化氮合酶含量升高，总抗氧化能力、谷胱甘肽过氧化物酶、过氧化氢酶、超氧化物歧化酶活性降低，NF-κB、环氧合酶2表达升高。这些结果表明，低硒通过氧化应激激活 NF-κB 通路诱导 M1/M2 失衡，加重热应激引起的肺组织炎症。本研究为从M1/M2角度探索硒缺乏引起的各类炎症的发病机制提供了理论依据，并为此类疾病的预防提供了参考。和诱导型一氧化氮合酶含量，总抗氧化能力、谷胱甘肽过氧化物酶、过氧化氢酶和超氧化物歧化酶的活性降低，NF-κB和环氧合酶2的表达增加。这些结果表明，低硒通过氧化应激激活 NF-κB 通路诱导 M1/M2 失衡，加重热应激引起的肺组织炎症。本研究为从M1/M2角度探索硒缺乏引起的各类炎症的发病机制提供了理论依据，并为此类疾病的预防提供了参考。和诱导型一氧化氮合酶含量，总抗氧化能力、谷胱甘肽过氧化物酶、过氧化氢酶和超氧化物歧化酶的活性降低，NF-κB和环氧合酶2的表达增加。这些结果表明，低硒通过氧化应激激活 NF-κB 通路诱导 M1/M2 失衡，加重热应激引起的肺组织炎症。本研究为从M1/M2角度探索硒缺乏引起的各类炎症的发病机制提供了理论依据，并为此类疾病的预防提供了参考。这些结果表明，低硒通过氧化应激激活 NF-κB 通路诱导 M1/M2 失衡，加重热应激引起的肺组织炎症。本研究为从M1/M2角度探索硒缺乏引起的各类炎症的发病机制提供了理论依据，并为此类疾病的预防提供了参考。这些结果表明，低硒通过氧化应激激活 NF-κB 通路诱导 M1/M2 失衡，加重热应激引起的肺组织炎症。本研究为从M1/M2角度探索硒缺乏引起的各类炎症的发病机制提供了理论依据，并为此类疾病的预防提供了参考。