Study Of The Effect Of Chronic Alcohol Consumption On Two Mouse Models Of Inflammatory Skin Diseases

Objective:The literature reports high rates of alcohol abuse in populations with inflammatory skin diseases,mainly including psoriasis,eczema,and seborrheic dermatitis.Clinical findings suggest that psoriasis patients who drink alcohol have lesions more often located in folds such as the axillae and groin,which are also locations where fungal fixations are more abundant.Epidemiological investigations have shown that alcohol abuse is a risk factor for seborrheic dermatitis.The role of Malassezia in seborrheic dermatitis has been relatively well established,and psoriasis patients who drink alcohol also have abundant Malassezia fixations in the fold lesions.It is speculated whether some interaction between the organism and Malassezia occurs in patients who drink alcohol,which disrupts the symbiotic homeostasis between Malassezia and the organism,leading to skin inflammation.In this study,two mouse models were constructed on alcohol-drinking mice:psoriasis model and seborrheic dermatitis-like mouse model,to investigate whether the combined effect of both alcohol consumption and Malassezia affects skin inflammation in mice,and to try to investigate the mechanism of hacat cell proliferation stimulated by ethanol and Malassezia in vitro initially.Methods:This study was divided into two parts:animal experiments and cellular experiments.Animal experiments were divided into two parts,1:the effect of alcohol consumption and Malassezia on psoriasis mouse model.The mice were chronically consumed alcohol for 4 weeks,and imiquimod was used in the mouse dorsal induction psoriasis model to observe the lesion performance and score,and HE staining was done to observe the pathological changes in the dorsal lesion sections,and the weight changes of the mice before and after modeling were recorded.The effect of alcohol consumption on Malassezia-induced dermatitis model in mice.After chronic alcohol consumption,the skin barrier was disrupted by tape application,and then the skin inflammation was induced by topical application of Malassezia suspension,and the dermatitis phenotype was observed.morphological characteristics.The proliferation of hacat cells after in vitro stimulation under different conditions was examined in the cellular assay section.hacat cell proliferation was detected by the CCK8 method and EDU method using different concentrations of ethanol,ethanol shared with Malassezia,and ethanol pretreated Malassezia supernatant added to hacat cell culture medium,respectively.Results:1.Alcohol consumption and topical application of Malassezia suspension did not aggravate PASI scores and lesion pathology in a mouse model of psoriasis.Chronic alcohol consumption led to weight loss and spleen shrinkage during imiquimod modeling,and consumption of higher concentrations of ethanol(20%)led to wasting and death during modeling.2.Chronic alcohol consumption led to heavier lesions and more pronounced epidermal thickening in the Malassezia-induced dermatitis model.The severity of Malassezia-induced dermatitis phenotype was correlated with the duration of alcohol consumption and the degree of skin barrier disruption,and the longer the duration of chronic alcohol consumption and the greater the degree of skin barrier disruption,the more severe the dermatitis in mice.Mice in the alcohol drinking group had higher transdermal water loss values,larger subcutaneous fat layer staining area,higher splenic index,and more active cell proliferation in the basal layer after modeling.3.In vitro stimulation with ethanol did not promote hacat cell proliferation,and in vitro stimulation with ethanol and Malassezia co-stimulation and ethanol pretreated Malassezia exocrine did not promote hacat cell proliferation.Conclusions:1.Alcohol consumption and topical application of Malassezia suspension did not aggravate the severity of skin lesions in a mouse model of psoriasis,but alcohol consumption led to weight loss and decreased splenic index,and alcohol consumption led to death during modeling.2.Alcohol consumption led to more severe skin lesions in a mouse model of Malassezia-induced dermatitis,and the aggravation of dermatitis was related to the duration of alcohol consumption and the degree of skin barrier disruption;the specific mechanism of dermatitis aggravation involved The specific mechanism for the exacerbation of dermatitis may involve the disruption of skin barrier function,abnormal cell proliferation in the basal layer,and the inflammatory response caused by the invasion of Malassezia into the epidermis.3.In vitro stimulation of hacat cells with ethanol and Malassezia did not reveal any change in cell proliferation.