This team aims to understand how various environmental stress caused by lifestyle change affect the inflammatory regulatory mechanisms at tissue/cellular levels. At the present, we analyze the inflammatory or oxidative stress response to various environmental components (e.g. bacteria, bacterial components, exercise-training, food components) using animal models of the aging and metabolic syndrome. In order to explore new biomarkers for early prediction or therapy monitoring of lifestyle related-disease risk, we also try to characterize a stress-induced molecule or a stress-related substance by metabolomic and proteomic analysis.

Obesity is a significant risk factor for developing type II diabetes, which has been attributed to chronic low-grade inflammation occurring in the adipose tissue of obese individuals. Now, we try to illuminate the role of mast cells in the adipose tissue for the pathogenesis of type II diabetes. Especially, we characterize the role of mast cell-derived bioactive substances in the differentiation and maturation of adipose cells for understanding the inflammation or neoangiogenesis in the adipose tissue. Furthremore, we evaluate the effect of exercise training on several inflammation-associated changes in adipose tissue, including infiltration of inflammatory macrophages and T cells.

Recently, it have been widely accepted that the body's circadian rhythms have a major influence on allergic disease including its symptoms, diagnosis, and treatment. Now, we try to understand the relationship between the itch intensity and circadian rhythm in spontaneous mouse model of atopic dermatitis for the enhancement of the therapeutic efficacy of resistant atopic dermatitis.

Chronic inflammation caused by various environmental stimuli (e.g. allergen, infection, nutrient excess or deficiency, radiation-induced DNA-damage) is a well-recognized risk factor for the induction and progression of cancers, such as gastric and liver cancers. In order to elucidate the pathogenesis of a chronic inflammation-mediated tumorigenesis, life-related diseases, other refractory diseases, we are characterizing whether these environmental stress alters a cell turnover or epigenome in a gastric tissue.

Commensal bacteria colonized symbiotically in our body are closely related to the human health and disease. The mucosal epithelium is continuously exposed to the antigen- and microbe-rich environment. Nevertheless, numerous commensal bacteria do not elicit the immune inflammation. Thus, it is hypothesized that the mucosal epithelial cells may equip with the mechanism to prevent or limit activation of immune inflammation and fortify the epithelial barrier function through host-microbe interactions, and this interaction plays role in the maintenance of intestinal epithelial homeostasis. Then, we take up the investigation to unlock the mechanism to maintain the gut homeostasis through host-microbe interactions.