Nanto-Hara Fumika, Yamazaki Makoto, Murakami Hitoshi, Ohtsu Haruhiko
Division of Meat Animal and Poultry Research, Institute of Livestock and Grassland Science, National Agriculture and Food Research Organization (NILGS), 2 Ikenodai, Tsukuba, Ibaraki, 305-0901, Japan.
J Anim Sci Biotechnol. 2023 Jun 3;14(1):81. doi: 10.1186/s40104-023-00878-5.
Heat stress in laying hens negatively affects egg production and shell quality by disrupting the homeostasis of plasma calcium and phosphorus levels. Although the kidney plays an important role in calcium and phosphorus homeostasis, evidence regarding the effect of heat stress on renal injury in laying hens is yet to be elucidated. Therefore, the aim of this study was to evaluate the effects of chronic heat stress on renal damage in hens during laying periods.
A total of 16 white-leghorn laying hens (32 weeks old) were randomly assigned to two groups (n = 8). One group was exposed to chronic heat stress (33 °C for 4 weeks), whereas the other group was maintained at 24 °C.
Chronic heat exposure significantly increased plasma creatinine and decreased plasma albumin levels (P < 0.05). Heat exposure also increased renal fibrosis and the transcription levels of fibrosis-related genes (COLA1A1, αSMA, and TGF-β) in the kidney. These results suggest that renal failure and fibrosis were induced by chronic heat exposure in laying hens. In addition, chronic heat exposure decreased ATP levels and mitochondrial DNA copy number (mtDNA-CN) in renal tissue, suggesting that renal mitochondrial dysfunction occurs under conditions of heat stress. Damaged mitochondria leak mtDNAs into the cytosol and mtDNA leakage may activate the cyclic GMP-AMP synthase (cGAS) stimulator of interferon genes (STING) signaling pathway. Our results showed that chronic heat exposure activated the cGAS-STING pathway as indicated by increased expression of MDA5, STING, IRF7, MAVS, and NF-κB levels. Furthermore, the expression of pro-inflammatory cytokines (IL-12) and chemokines (CCL4 and CCL20) was upregulated in heat-stressed hens.
These results suggest that chronic heat exposure induces renal fibrosis and mitochondrial damage in laying hens. Mitochondrial damage by heat stress may activate the mtDNA-cGAS-STING signaling and cause subsequent inflammation, which contributes to the progression of renal fibrosis and dysfunction.
蛋鸡热应激通过破坏血浆钙和磷水平的稳态，对产蛋性能和蛋壳质量产生负面影响。尽管肾脏在钙和磷稳态中起重要作用，但热应激对蛋鸡肾脏损伤影响的相关证据仍有待阐明。因此，本研究的目的是评估慢性热应激对产蛋期母鸡肾脏损伤的影响。
总共16只白来航母鸡（32周龄）被随机分为两组（n = 8）。一组暴露于慢性热应激（33°C，持续4周），而另一组维持在24°C。
慢性热暴露显著增加了血浆肌酐水平，降低了血浆白蛋白水平（P < 0.05）。热暴露还增加了肾脏纤维化以及肾脏中纤维化相关基因（COLA1A1、αSMA和TGF-β）的转录水平。这些结果表明，慢性热暴露诱导了蛋鸡肾衰竭和纤维化。此外，慢性热暴露降低了肾脏组织中的ATP水平和线粒体DNA拷贝数（mtDNA-CN），表明在热应激条件下发生了肾脏线粒体功能障碍。受损的线粒体将mtDNA泄漏到细胞质中，mtDNA泄漏可能激活干扰素基因（STING）信号通路的环磷酸鸟苷-腺苷酸合成酶（cGAS）刺激物。我们的结果表明，慢性热暴露激活了cGAS-STING通路，表现为MDA5、STING、IRF7、MAVS和NF-κB水平的表达增加。此外，热应激母鸡中促炎细胞因子（IL-12）和趋化因子（CCL4和CCL20）的表达上调。
这些结果表明，慢性热暴露诱导蛋鸡肾脏纤维化和线粒体损伤。热应激引起的线粒体损伤可能激活mtDNA-cGAS-STING信号并导致随后的炎症，这有助于肾脏纤维化和功能障碍的进展。
