Alterations in ambient temperature have been associated with multiple detrimental effects on broilers such as intestinal barrier disruption and dysbiosis resulting in systemic inflammation. Inflammation and 25-hydroxycholecalciferol (25-OH-D3) have shown to play a negative and positive role, respectively, in the regulation of bone mass. Hence the potential of 25-OH-D3 in alleviating heat induced bone alterations and its mechanisms was studied. Heat stress (HS) directly induced a decrease in tibia material properties and bone mass, as demonstrated by lower mineral content, and HS caused a notable increase in intestinal permeability. Treatment with dietary 25-OH-D3 reversed the HS-induced bone loss and barrier leak. Broilers suffering from HS exhibited dysbiosis and increased expression of inflammatory cytokines in the ileum and bone marrow, as well as increased osteoclast number and activity. The changes were prevented by dietary 25-OH-D3 administration. Specifically, dietary 25-OH-D3 addition decreased abundance of B- and T-cells in blood, and the expression of inflammatory cytokines, especially TNF-α, in both the ileum and bone marrow, but did not alter the diversity and population or composition of major bacterial phyla. With regard to bone remodeling, dietary 25-OH-D3 supplementation was linked to a decrease in serum C-terminal cross-linked telopeptide of type I collagen reflecting bone resorption and a concomitant decrement in osteoclast-specific marker genes expression (e.g. cathepsin K), whereas it did not apparently change serum bone formation markers during HS. These data underscore the damage of HS to intestinal integrity and bone health, as well as that dietary 25-OH-D3 supplementation was identified as a potential therapy for preventing these adverse effects.

中文翻译：

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25-羟基胆钙化醇可逆转热诱导的育肥肉鸡骨骼质量变化，这些变化与肠道完整性和炎症相关

环境温度的变化与对肉鸡的多种不利影响有关，例如肠道屏障破坏和生态失调导致全身炎症。炎症和 25-羟基胆钙化醇 (25-OH-D3) 已显示分别在骨量调节中发挥消极和积极作用。因此，研究了 25-OH-D3 在减轻热诱导骨改变方面的潜力及其机制。热应激 (HS) 直接导致胫骨材料特性和骨量减少，如矿物质含量降低所证明的那样，并且 HS 导致肠道通透性显着增加。膳食 25-OH-D3 治疗逆转了 H2S 诱导的骨质流失和屏障渗漏。患有HS的肉鸡表现出生态失调和回肠和骨髓中炎性细胞因子的表达增加，以及破骨细胞数量和活性增加。膳食 25-OH-D3 给药可防止这些变化。具体而言，饮食中添加 25-OH-D3 降低了血液中 B 细胞和 T 细胞的丰度，以及回肠和骨髓中炎性细胞因子，尤其是 TNF-α 的表达，但没有改变多样性和种群或主要细菌门的组成。关于骨重塑，膳食补充 25-OH-D3 与反映骨吸收的 I 型胶原的血清 C 端交联端肽的减少和破骨细胞特异性标记基因表达（例如组织蛋白酶 K）的伴随减少有关，而它在 HS 期间没有明显改变血清骨形成标志物。这些数据强调了 HS 对肠道完整性和骨骼健康的损害，