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.