Long-chain saturated fatty acids in breast milk are associated with the pathogenesis of atopic dermatitis via induction of inflammatory ILC3s

Autor:	Yoichi Kohno, Naoki Shimojo, Weng Sheng Kong, Masamoto Kanno, Naohiro Tsuyama, Asako Nobukiyo, Makoto Arita, Sho Mokuda, Kazutaka Ikeda, Fumiya Yamaide, Yun Guo, Nobuhiro Nakatani, Hiroshi Ohno, Hiroko Inoue, Yumiko Nakanishi, Taiji Nakano
Jazyk:	angličtina
Rok vydání:	2021
Předmět:	Male 0301 basic medicine Chemokine Science Innate lymphoid cells Gut flora Breast milk Article Dermatitis Atopic Mice 03 medical and health sciences 0302 clinical medicine Immune system medicine Alarmins Animals Metabolomics Prospective Studies Atopic dermatitis Skin Multidisciplinary Innate immune system Milk Human biology Interleukins Fatty Acids Interleukin-17 Innate lymphoid cell biology.organism_classification Acquired immune system medicine.disease Experimental models of disease Disease Models Animal Milk 030104 developmental biology Immunology biology.protein Medicine Female 030215 immunology
Zdroj:	Scientific Reports, Vol 11, Iss 1, Pp 1-22 (2021) Scientific Reports
ISSN:	2045-2322
Popis:	Breastfeeding influences the immune system development in infants and may even affect various immunological responses later in life. Breast milk provides a rich source of early nutrition for infant growth and development. However, the presence of certain compounds in breast milk, related to an unhealthy lifestyle or the diet of lactating mothers, may negatively impact infants. Based on a cohort study of atopic dermatitis (AD), we find the presence of damage-associated molecular patterns (DAMPs) activity in the mother’s milk. By non-targeted metabolomic analysis, we identify the long-chain saturated fatty acids (LCSFA) as a biomarker DAMPs (+) breast milk samples. Similarly, a mouse model in which breastfed offspring are fed milk high in LCSFA show AD onset later in life. We prove that LCSFA are a type of damage-associated molecular patterns, which initiate a series of inflammatory events in the gut involving type 3 innate lymphoid cells (ILC3s). A remarkable increase in inflammatory ILC3s is observed in the gut, and the migration of these ILC3s to the skin may be potential triggers of AD. Gene expression analysis of ILC3s isolated from the gut reveal upregulation of genes that increase ILC3s and chemokines/chemokine receptors, which may play a role in ILC migration to the skin. Even in the absence of adaptive immunity, Rag1 knockout mice fed a high-LCSFA milk diet develop eczema, accompanied by increased gut ILC3s. We also present that gut microbiota of AD-prone PA milk-fed mice is different from non-AD OA/ND milk-fed mice. Here, we propose that early exposure to LCSFAs in infants may affect the balance of intestinal innate immunity, inducing a highly inflammatory environment with the proliferation of ILC3s and production of interleukin-17 and interleukin-22, these factors may be potential triggers or worsening factors of AD.
Databáze:	OpenAIRE
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