Abstract
Some lactic acid bacteria (LAB) are known to improve atopic dermatitis (AD) through the regulation and stimulation of the host immune system. In this study, we found that ingestion of yogurt containing Lactococcus lactis 11/19-B1 strain (L. lactis 11/19-B1) daily for 8 weeks significantly improved the severity scoring of atopic dermatitis (SCORAD) system score from 38.8 ± 14.4 to 24.2 ± 12.0 in children suffering from AD. We tried to identify which LAB species among the five species contained in the test yogurt contributed to the improvement in AD pathology using an AD mouse model induced by repeated application of 1-fluoro-2, 4-dinitrobenzene (DNFB). AD-like skin lesions on the dorsal skin and ear were most improved by L. lactis 11/19-B1 intake among the five LAB species. In addition, analysis of CD4+ T cell subsets in Peyer’s patches (PPs) and cervical lymph nodes (CLNs) indicated that the intake of L. lactis 11/19-B1 generally suppressed all subsets related to inflammation, i.e., Th1, Th2 and Th17, instead of activating the suppressive system, Treg, in the AD mouse model. Histological observations showed ingestion of L. lactis 11/19-B1 significantly suppressed severe inflammatory findings, such as inflammatory cell filtration, epidermal erosion and eosinophil infiltration. These results suggest that the immunomodulatory effects of L. lactis 11/19-B1 contribute to improvements in AD pathology.
Highlights
atopic group (Atopic) dermatitis (AD) is a chronic inflammatory skin disease characterized by repeated episodes of exacerbation and remission
We investigated the anti-allergic activities and related mechanisms of L. lactis 11/19-B1 using a mouse atopic dermatitis (AD) model induced by the repeated application of 1-fluoro-2, 4-dinitrobenzene (DNFB)
Biomarkers IgE, thymus and activation-regulated chemokine (TARC), LDH and EOS, which reflect the pathology of AD, and other biochemical data did not differ between before and after the test yogurt intake
Summary
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by repeated episodes of exacerbation and remission. Many AD patients have an atopic predisposition, and frequent skin damage associated with itching results in a decreased quality of life [1]. The etiology of AD involves the disruption of skin barrier function and immune abnormalities, which influence each other and affect the pathogenesis and progression of the disease. In terms of the immunological abnormalities of AD, in particular T cell subset composition, such as Th1, Th2 and Th17, and changes in subset-specific. Nutrients 2020, 12, 763 cytokines participate in the genesis of the disease. Th17 cells, which play an important role in the pathogenesis of psoriasis and production of certain cytokines from keratinocytes, were observed in the peripheral blood of AD patients [4]
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