Biomedical Center for Animal Resource and Development, Seoul National University College of Medicine, Seoul 110-799, Republic of Korea.
J Dermatol Sci. 2013 Dec;72(3):225-32. doi: 10.1016/j.jdermsci.2013.07.004. Epub 2013 Jul 23.
The interleukin 10 deficient mice (IL-10(-/-)) showed high incidence of pup alopecia compared to other strains, and pup alopecia was caused by skin inflammation and was recoverable. Pup alopecia of B6.IL-10(-/-) might be related with maternal factor and interleukin-10 deficient phenotype.
The objectives of this study were elucidating of maternal factors for inflammatory milk production and characterization of pup alopecia in IL-10(-/-) mice.
Incidences of pup alopecia were analyzed with 13 breeding cases. Comparison between control and alopecia pups and its dams, were conducted with histological examination (H&E, TUNEL assay, immunohistochemistry for F4/80, iNOS, CD206, Gr-1, CD4, CD8, CD11c and CD326), fostering test, forced weaning test, qPCR for tyrosine hydroxylase, flow cytometry, IL-10 inhibition test, BMDM stimulation test and LC/MS analysis.
Presence of pregnancy in postpartum estrus showed significant correlation with inflammatory milk production and mammary gland involution in B6.IL-10(-/-) mice. There were no different mass in inflammatory milk, but different ionization intensity was detected. Inflammatory milk directly induced hepatocyte steatosis, catagen stage specific hair breaking and alopeicia in pups. Histologically, hypertropy of outer root sheath and macrophage/neutrophil infiltration were typical.
B6.IL-10(-/-) dam with stress such as PPE could produce untimely mammary gland involution and inflammatory milk production. Interleukin 10 is important for maternal stress regulation and protecting inflammatory milk production, also influence severity of pup skin inflammation and alopecia. Remarkably, inflammatory milk induced hepatocyte steatosis, and it could indicate there is abnormal lipid metabolism. This was first report for catagen specific alopecia in mouse.
与其他品系相比，白细胞介素 10 缺陷小鼠（IL-10(-/-)）的幼仔脱毛发生率较高，且幼仔脱毛是由皮肤炎症引起的，可恢复。B6.IL-10(-/-)幼仔脱毛可能与母体因素和白细胞介素 10 缺陷表型有关。
本研究旨在阐明引起炎症性乳汁产生的母体因素，并对 IL-10(-/-)小鼠的幼仔脱毛进行特征描述。
通过 13 个繁殖案例分析幼仔脱毛的发生率。通过组织学检查（H&E、TUNEL 检测、F4/80、iNOS、CD206、Gr-1、CD4、CD8、CD11c 和 CD326 的免疫组化）、寄养试验、强制断奶试验、酪氨酸羟化酶 qPCR、流式细胞术、白细胞介素 10 抑制试验、BMDM 刺激试验和 LC/MS 分析，比较对照组和脱毛组及其母鼠之间的差异。
产后发情期妊娠的存在与 B6.IL-10(-/-)小鼠的炎症性乳汁产生和乳腺退化有显著相关性。炎症性乳汁的质量没有差异，但检测到不同的离子强度。炎症性乳汁直接诱导仔鼠肝细胞脂肪变性、毛发生长周期特定的毛发断裂和脱毛。组织学上，外根鞘肥大和巨噬细胞/中性粒细胞浸润是典型特征。
处于 PPE 等应激状态下的 B6.IL-10(-/-)母鼠可能会导致乳腺退化和炎症性乳汁产生异常。白细胞介素 10 对母体应激调节和保护炎症性乳汁产生非常重要，也会影响仔鼠皮肤炎症和脱毛的严重程度。值得注意的是，炎症性乳汁诱导肝细胞脂肪变性，这表明存在异常的脂质代谢。这是首次报道小鼠的退行期特异性脱毛。
