Raw data file in postbiotic impact of pasteurized L. reuteri to atopic dermatitis with dysbiosis

The "gut-skin axis" has highlighted, but has not found whether atopic dermatitis (AD) develops from colitis. In male NC/Nga mice, high sensitivity to dextran sulfate sodium (DSS)-induced colitis was found, 5 to 8 weeks later, AD-like lesions with “itching” developed spontaneously at specific bilateral symmetric sites, inducing enhanced blood IgE and basophils, elevated Th17 and ILC2 in lymph nodes enlarged, and increased cutaneous mast cells. Gut motility disorders after DSS-induced colitis caused dysbiosis by bacteria such as Escherichia coli, Enterococcus faecalis, Bacteroides acidifaciens. But even after the colitis subsided, dysbiosis extended by bacteria such as Bacteroides acidifaciens, Streptococcus danieliae, Mucispirillum schaedleri, Enterorhabdus mucosicola. AD-sign “itching” depended on histamine-secreted mast cells increased by IL-33 produced from gut epithelium in dysbiosis, but not on IL-31, "itchy" cytokine. It was suggested that postbiotic impact of pasteurized Limosilactobacillus reuteri-suspension may suppress high serum IL-33 by improving dysbiosis, resulted in relieving “itching” and cured AD.