Reduced Fecal Calprotectin and Inflammation in a Murine Model of Atopic Dermatitis Following Probiotic Treatment

• Published in: International journal of molecular sciences Vol. 21; no. 11; p. 3968
• Main Authors: Kim, Myoung-Ju, Kim, Ji-Young, Kang, Minje, Won, Moo-Ho, Hong, Seok-Ho, Her, Young
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 31.05.2020; MDPI
• Subjects: Administration, Oral; Allergens; Allergies; Animal models; Animals; Atopic dermatitis; atopy; calprotectin; Cytokines; Cytokines - metabolism; Dermatitis; Dermatitis, Atopic - microbiology; Dermatitis, Atopic - therapy; Disease Models, Animal; Dysbacteriosis; Eczema; Feces; Feces - chemistry; Female; Gastrointestinal Microbiome; Homeostasis; Immunoglobulin E; Immunology; Inflammation; Inflammation - metabolism; Inflammatory bowel disease; Intestine; Leukocyte L1 Antigen Complex - metabolism; Lipids; Mice; Pathogenesis; Polymerase Chain Reaction; Probiotics; Probiotics - pharmacology; Proteins; Pruritus; Pruritus - metabolism; Recurrence; Skin - metabolism; Skin diseases; Skin lesions; atopy; inflammation; calprotectin; probiotics
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21113968

Atopic dermatitis (AD) is one of the most common skin diseases with inflammation, chronic relapses, and intense pruritus. Its pathogenesis includes genetic susceptibility, an abnormal epidermal lipid barrier, and an increased production of IgE due to immune dysregulation. Recently, AD has been reported to be associated with intestinal inflammation and dysbiosis in human and murine models. Various probiotics are being used to control intestinal dysbiosis and inflammatory reactions. However, it is difficult to predict or determine the therapeutic effects of the probiotics, since it is rare for clinicians to use the probiotics alone to treat AD. It is also difficult to check whether the intestinal inflammation in patients with AD has improved since probiotic treatment. The aim of the present study was to determine whether mice with induced atopic dermatitis had any changes in fecal calprotectin, an indicator of intestinal inflammation, after probiotic administration. Our results showed that the fecal calprotectin levels in mice with induced dermatitis decreased significantly after the administration of probiotics. In addition, epidermal skin lesions were attenuated and inflammatory-related cytokines were downregulated after the administration of probiotics in mice with induced dermatitis. These results suggest that changes in fecal calprotectin levels could be used to assess the effectiveness of a probiotic strain as an adjuvant treatment for AD.