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    Home > Active Ingredient News > Immunology News > J Allergy Kleinol: Skin flora regulates skin and lung allergic inflammation.

    J Allergy Kleinol: Skin flora regulates skin and lung allergic inflammation.

    • Last Update: 2020-08-11
    • Source: Internet
    • Author: User
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    Newborns are exposed to environmental factors, including microorganisms and allergens, immediately after birth.
    these exposures occur at the same time as the mature immune system and affect them, leading to susceptibility and development of the disease.
    microbes are exposed to the development of immune steady state in the lungs and intestines. changes in the composition of
    microorganisms or the absence of the microbiome can lead to immune development disorders, thereby increasing sensitivity to and increasing the occurrence of reactive diseases.
    skin provides a physical barrier to the environment and outer layer, the epidermis, which is formed by terminal lysic cells and lipids.
    epidermis differentiation and changes in lipid composition can lead to impaired skin barrier function, which increases the permeability and permeability of environmental factors such as allergens.
    the antigen-infused cells (APCs) in the skin transport antigens to the lymph nodes, where they activate T cells, and in addition, the reactivation of the active T cells in the skin tissue is essential so that The T-cells can perform their effects at that site.
    long known as The LCs, which are present in the epidermis, are considered to be the main type of APC in the skin.
    However, other APCs such as macrophages and traditional dendritic cells (dc) cDC1 and cDC2 are clearly present in the dermis and can present antigens to local T cells.
    the development of allergen allergen allergens through the skin that can lead to allergic skin inflammation or allergic dermatitis.
    -specific dermatitis occurs mainly in childhood.
    for most children, the inflammation is short-lived and disappears when they grow up;
    Although studies have shown that the age of onset of the disease and the severity of the disease play a role in determining whether allergic skin inflammation continues into adulthood, the parameters for determining the sustainability of the disease remain unclear.
    study sheds light on the fundamentals of allergic inflammation in different tissues and highlights possible early opportunities for the prevention of allergic diseases.
    microbes are exposed to early life and affect the development of the immune system.
    the authors assessed the importance of the skin microbiome for the development of the skin's immune environment.
    the main coordinate analysis (PCoA) of longitudinal sampling of skin microbiomes from birth to adulthood in mice showed that the composition of the skin microbiome at a particular point in time after birth of different mice was more similar than that of a particular animal at different ages.
    in addition, stratified clusters of samples based on relative genus abundance showed similarities between the skin microbiome on day 2 and adult mice.
    in assessing the diversity of the skin microbiome and the function of the skin barrier, the authors observed a negative correlation between bacterial diversity and impaired skin barrier function.
    , these results show that the diversity of the skin microbiome is important for building the skin barrier.
    To further assess the importance of microbiome in the development of the skin immune environment, the authors conducted transcriptional analysis of immature skin from adult SPF and GF mice.
    skin microbiome not only plays an important role in the development of the skin immune environment, but also plays an important role in the skin's barrier function.
    results showed that after birth, the microbiome drives the production of chemo-factors and APCs are inoculated in the skin.
    allergic skin inflammation is usually characterized by changes in the composition of the skin's micro-organisms, while patients with aspecific dermatitis are often infected with Staphylococcus aureus.
    the authors determined whether epidermis in newborn and adult mice should alter the skin microbiome. The main coordinated analysis of the
    showed that the skin microbiome of newborn mice after allergization was different from that of adult mice.
    these data, skin inflammation creates a habitat suitable for Staphylococcus aureus.
    to assess the effects of live Staphylococcus aureus exposure on allergic skin inflammation, the authors exposed newborn mice to Staphylococcus aureus in the first week after epithelial HDM sensitivity.
    staphylococcus aureus increases the severity of skin disease, while the skin barrier function is not significantly impaired.
    , an analysis of the composition of skin immune cells showed a significant decrease in the frequency of eosinophils and an increase in the number of neutrophils.
    here, the authors used experimental models of primary and adult epidermal allergy to determine immune rules that control skin inflammation in early life.
    the authors found that the nature and severity of allergic skin inflammation varied with age.
    the skin should become primary allergens, after the lung irritation, the skin and lungs of adult mice showed a mixed th2/Th17 inflammatory response, while the newborn mice's lungs showed a Th2-based inflammatory response, without a significant skin inflammation response.
    analysis of the original skin tissue showed that before the formation of the skin microbiome, the skin showed impaired the production of chemofactors and alarm proteins and a decrease in the number of skin resident APCs.
    the formation of microbiomes drives the generation of chemo-factors, APCs vaccination and the resulting immunity maturation.
    after this maturation process, mature skin antigen-raised cells are able to locate inflammation at the exposed site, i.e. the skin, and cause significant allergic skin inflammation.
    in general, these results suggest that early skin immunity matures, at least in part, dependent on microbial exposure, and that the manifestations of the disease are determined by the maturation of the barrier tissue.
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