Intestinal inflammation can be accompanied by osteoporosis, but their relationship, mediated by immune responses, remains unclear. Here, we investigated a non-IgE-mediated food-allergic enteropathy model of ovalbumin (OVA) 23-3 mice expressing OVA-specific T-cell-receptor transgenes. Mesenteric lymph nodes (MLNs) and their pathogenic CD4⁺T cells were important to enteropathy occurrence and exacerbation when the mice were fed an egg-white (EW) diet. EW-fed OVA23-3 mice also developed bone loss and increased CD44^hiCD62L^loCD4⁺T cells in the MLNs and bone marrow (BM); these changes were attenuated by MLN, but not spleen, resection. We fed an EW diet to F1 cross offspring from OVA23-3 mice and a mouse line expressing the photoconvertible protein KikGR to track MLN CD4⁺T cells. Photoconverted MLN CD44^hiCD62L^loCD4⁺T cells migrated predominantly to the BM; pit formation assay proved their ability to promote bone damage via osteoclasts. Significantly greater expression of IL-4 mRNA in MLN CD44^hiCD62L^loCD4⁺T cells and bone was observed in EW-fed OVA23-3 mice. Anti-IL-4 monoclonal antibody injection canceled bone loss in the primary inflammation phase in EW-fed mice, but less so in the chronic phase. This novel report shows the specific inflammatory relationship, via Th2-dominant-OVA-specific T cells and IL-4 production, between MLNs and bone, a distant organ, in food-allergic enteropathy.

肠道炎症可伴有骨质疏松症，但它们之间由免疫反应介导的关系仍不清楚。在这里，我们研究了一种非 IgE 介导的食物过敏性肠病模型，该模型是表达 OVA 特异性 T 细胞受体转基因的卵清蛋白 (OVA) 23-3 小鼠。当给小鼠喂食蛋清 (EW) 饮食时，肠系膜淋巴结 (MLN) 及其致病性 CD4 ^{+ T 细胞对肠病的发生和恶化很重要。}EW 喂养的 OVA23-3 小鼠也出现骨质流失并增加 CD44 ^hi CD62L ^lo CD4 ⁺MLN 和骨髓 (BM) 中的 T 细胞；这些变化因 MLN 而不是脾脏切除而减弱。我们用 EW 饮食喂养 OVA23-3 小鼠的 F1 杂交后代和表达光转换蛋白 KikGR 的小鼠系以追踪 MLN CD4 ⁺ T 细胞。光转化的MLN CD44 ^hi CD62L ^lo CD4 ⁺ T 细胞主要迁移到 BM；凹坑形成试验证明了它们能够通过破骨细胞促进骨损伤。^{MLN CD44 hi} CD62L ^lo CD4 ⁺中 IL-4 mRNA 的表达显着增加在 EW 喂养的 OVA23-3 小鼠中观察到 T 细胞和骨骼。抗 IL-4 单克隆抗体注射消除了 EW 喂养小鼠原发性炎症期的骨质流失，但在慢性期则较少。这份新报告显示了食物过敏性肠病中 MLN 和远处器官骨骼之间通过 Th2 显性 OVA 特异性 T 细胞和 IL-4 产生的特定炎症关系。