D-galactose Intake Alleviates Atopic Dermatitis in Mice by Modulating Intestinal Microbiota

Abstract

Atopic dermatitis (AD) is one of the most prevalent, chronic and persistent inflammatory skin diseases closely associated with intestinal microbiota. To evaluate the effect of D-galactose intake on AD, we orally administered D-galactose to BALB/c mice whose ears and skin were treated with 2,4-dinitrochlorobenzene (DNCB). D-galactose alleviated DNCB-induced AD-like phenotypes such as redness, scaling/dryness and excoriation. Ear thickness was also decreased by D-galactose administration. Histopathological analysis revealed decreased epidermal thickening, infiltration of immune cells, especially mast cells, in the dermis. Total levels of serum IgE representing the immunological response of AD were decreased by D-galactose administration. Microbiota analysis showed that D-galactose administration restored gut microbiota profiles, which were altered in AD mice, characterized by increased abundance of Bacteroidetes and decreased abundance of Firmicutes. The increased abundance of Bacteroides and the decreased abundance of Prevotella and Ruminococcus were reversed by D-galactose treatment, following improvement of AD. Our results suggest the possible use of D-galactose as a prebiotic to alleviate AD by altering gut microbiota.

The Effects of Saposhnikovia divaricata Aqueous Extracts on the Inflammation and Intestinal Microflora in Allergic Rhinitis Mice

“…Moreover, Burkholderia, which belonged to Proteobacteria, in intestinal contents of fish was increased by the growth- promoting traditional Chinese medicine treatment [45]. Kim's team reported that the abundance of Firmicutes was decreased when atopic dermatitis in mice was improved [46]. Similarly, this analysis of intestinal microflora in this study reported that those microflorae may play a role in the improvement of AR, which deserves further study.…”

D‐galactose might mediate some of the skeletal muscle hypertrophy‐promoting effects of milk—A nutrient to consider for sarcopenia?

“…[89] D-galactose has the potential to counteract both EPCs. Orally administered D-galactose can alleviate inflammation [90] and reduce oxidative stress [45,91] in rodents. Additionally, even trace amounts of galactose can rescue growth factor (IGF-1) signaling in vitro.…”

“…[ 64,65 ] Furthermore, D‐galactose can also counteract mechanisms responsible for low nutrient availability. At the organismic level, D‐galactose might promote gastrointestinal homeostasis [ 45,90–93 ] and improve the malabsorption of nutrients recognized as some of the causes of malnutrition in old age. [ 94,95 ] Additionally, galactose can replenish liver glycogen stores and provide a reserve for the maintenance of constant energy supply between meals, which are less frequent and provide fewer nutrients in the elderly.…”

Exploratory Study of Gastrointestinal Redox Biomarkers in the Presymptomatic and Symptomatic Tg2576 Mouse Model of Familial Alzheimer’s Disease: Phenotypic Correlates and Effects of Chronic Oral d-Galactose

“…Nevertheless, harmful effects of chronic D-galactose treatment are usually observed after parenteral administration of large doses, while chronic oral ad libitum administration has so far only been associated with beneficial effects in animal models of AD 25,26,32 and atopic dermatitis. 42 A large body of evidence suggests that the majority of the harmful and beneficial effects of D-galactose might be explained by tissue exposure. Peroral administration of D-galactose, associated with beneficial effects, usually results in 10-fold lower tissue exposure in comparison with parenteral routes due to intestinal absorption and liver retention.…”

“…Chronic parenteral administration of d -galactose is widely utilized for the induction of oxidative stress and modeling aging, , so its detrimental effects on redox homeostasis in wild-type animals are not surprising. Nevertheless, harmful effects of chronic d -galactose treatment are usually observed after parenteral administration of large doses, while chronic oral ad libitum administration has so far only been associated with beneficial effects in animal models of AD ,, and atopic dermatitis . A large body of evidence suggests that the majority of the harmful and beneficial effects of d -galactose might be explained by tissue exposure.…”