Allergology international : official journal of the Japanese Society of Allergology · 2026
Infant dermatitis induces long-lasting innate immune imprinting associated with the exacerbated adult atopic dermatitis-like skin inflammation.
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Sugiyama Hiroki, Tamari Masato, Hayashi Yuka, Nagano Naoko, Yamada Ayako, Orimo Keisuke, Saito Kyoko, Matsuoka Ryo, Motomura Kenichiro, Fujita Satoshi, Nakazaki Hisataka, Yamamoto Hiromichi, Higuchi Taro, Arae Ken, Ikutani Masashi, Yamaguchi Kiyoshi, Furukawa Yoichi, Ito Shuichi, Sudo Katsuko, Saito Hirohisa, Nakae Susumu, Matsumoto Kenji, Morita Hideaki
Аннотация
BACKGROUND: Atopic dermatitis (AD) frequently begins during infancy, and AD arising in early infancy represents a predictor of persistent AD. However, the mechanisms by which infantile skin inflammation programs future inflammatory susceptibility remain poorly understood.
METHODS: Two-week-old mice were treated with MC903 (vitamin D analogue) for 2 weeks and allowed to recover until adulthood. Topical corticosteroids were administered to a subset of mice after the induction of dermatitis during infancy. At 8 weeks of age, mice were rechallenged with MC903. Skin inflammation was evaluated by ear thickness, histological analysis, quantitative PCR, and flow cytometry. IL-4 and IL-5 reporter mice were used to identify the cellular sources of type 2 cytokines, and ILC populations were analyzed by uniform manifold approximation and projection.
RESULTS: MC903 application during infancy induced AD-like dermatitis with epidermal hyperplasia, increased type 2 cytokines, and infiltration of eosinophils, basophils, and ILCs. Mice experiencing infantile dermatitis developed markedly enhanced skin inflammation upon MC903 rechallenge in adulthood. Basophils were the major source of IL-4, whereas CCR6- ILCs produced IL-5. Infantile dermatitis resulted in the persistent expansion of Sca-1+CCR6- ILC populations. Notably, TSLP expression upon rechallenge was not increased in mice with a history of infantile dermatitis compared with controls. Although topical corticosteroid treatment reduced acute inflammation, it failed to prevent an exaggerated inflammatory response upon adult rechallenge.
CONCLUSIONS: Infantile skin inflammation establishes long-lasting innate immune imprinting that predisposes skin to exaggerated type 2 inflammation later in life. Under the condition tested, topical corticosteroid treatment did not attenuate this enhanced responsiveness.
METHODS: Two-week-old mice were treated with MC903 (vitamin D analogue) for 2 weeks and allowed to recover until adulthood. Topical corticosteroids were administered to a subset of mice after the induction of dermatitis during infancy. At 8 weeks of age, mice were rechallenged with MC903. Skin inflammation was evaluated by ear thickness, histological analysis, quantitative PCR, and flow cytometry. IL-4 and IL-5 reporter mice were used to identify the cellular sources of type 2 cytokines, and ILC populations were analyzed by uniform manifold approximation and projection.
RESULTS: MC903 application during infancy induced AD-like dermatitis with epidermal hyperplasia, increased type 2 cytokines, and infiltration of eosinophils, basophils, and ILCs. Mice experiencing infantile dermatitis developed markedly enhanced skin inflammation upon MC903 rechallenge in adulthood. Basophils were the major source of IL-4, whereas CCR6- ILCs produced IL-5. Infantile dermatitis resulted in the persistent expansion of Sca-1+CCR6- ILC populations. Notably, TSLP expression upon rechallenge was not increased in mice with a history of infantile dermatitis compared with controls. Although topical corticosteroid treatment reduced acute inflammation, it failed to prevent an exaggerated inflammatory response upon adult rechallenge.
CONCLUSIONS: Infantile skin inflammation establishes long-lasting innate immune imprinting that predisposes skin to exaggerated type 2 inflammation later in life. Under the condition tested, topical corticosteroid treatment did not attenuate this enhanced responsiveness.