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Abstract：
BACKGROUND: Although numerous studies have suggested a negative correlation between Helicobacter pylori (H. pylori) infection and allergies, there has been limited research on the relationship between H. pylori infections and atopic dermatitis (AD). The present study aimed to investigate the effects of H. pylori infection in an AD mouse model and identify potential mechanisms related to type 2 immunity, skin barrier defects, and pruritus.
METHODS: A model of AD-like symptoms was established with 2,4-dinitrochlorobenzene (DNCB) after infection of the gastric cavity with H. pylori. Analysis of the expression of key inflammatory cytokines and serum levels of immunoglobulin E (IgE) was based on enzyme-linked immunosorbent assay (ELISA). The expression of filaggrin (FLG) and loricrin (LOR) were analyzed by immunohistochemistry staining. The evaluation of STAT1, STAT3, phosphorylated STAT1 (phospho-STAT1), and phosphorylated STAT3 (phospho-STAT1) expression levels in skin lesions was performed using western blot.
RESULTS: The present study showed that the H. pylori-positive AD group (HP+AD+) exhibited milder skin lesions, including erythema, erosion, swelling, and scaling, than the H. pylori-negative AD group (HP-AD+). Additionally, HP+AD+ displayed lower levels of IgE in serum, and downregulated expression of interleukins 4 and 31 (IL-4 and IL-31) in serum. Furthermore, HP+AD+ demonstrated higher expression of filaggrin and loricrin than HP-AD+. Notably, H. pylori significantly reduced the amount of phosphorylated STAT1 and STAT3.
CONCLUSIONS: Helicobacter pylori infection negatively regulates the inflammatory response by affecting inflammatory factors in the immune response, and repairs the defective epidermal barrier function. In addition, H. pylori infection may reduce IL-31, thereby alleviating pruritus. These effects may be associated with the inhibition of JAK-STAT signaling activation.
METHODS: A model of AD-like symptoms was established with 2,4-dinitrochlorobenzene (DNCB) after infection of the gastric cavity with H. pylori. Analysis of the expression of key inflammatory cytokines and serum levels of immunoglobulin E (IgE) was based on enzyme-linked immunosorbent assay (ELISA). The expression of filaggrin (FLG) and loricrin (LOR) were analyzed by immunohistochemistry staining. The evaluation of STAT1, STAT3, phosphorylated STAT1 (phospho-STAT1), and phosphorylated STAT3 (phospho-STAT1) expression levels in skin lesions was performed using western blot.
RESULTS: The present study showed that the H. pylori-positive AD group (HP+AD+) exhibited milder skin lesions, including erythema, erosion, swelling, and scaling, than the H. pylori-negative AD group (HP-AD+). Additionally, HP+AD+ displayed lower levels of IgE in serum, and downregulated expression of interleukins 4 and 31 (IL-4 and IL-31) in serum. Furthermore, HP+AD+ demonstrated higher expression of filaggrin and loricrin than HP-AD+. Notably, H. pylori significantly reduced the amount of phosphorylated STAT1 and STAT3.
CONCLUSIONS: Helicobacter pylori infection negatively regulates the inflammatory response by affecting inflammatory factors in the immune response, and repairs the defective epidermal barrier function. In addition, H. pylori infection may reduce IL-31, thereby alleviating pruritus. These effects may be associated with the inhibition of JAK-STAT signaling activation.
摘要：
背景：尽管许多研究表明幽门螺杆菌（H.幽门螺杆菌)感染和过敏，关于幽门螺杆菌感染与特应性皮炎(AD)之间关系的研究有限.本研究旨在探讨H.pylori感染对AD小鼠模型的影响，并确定与2型免疫相关的潜在机制。皮肤屏障缺损,还有瘙痒.
方法：用2,4-二硝基氯苯（DNCB）感染幽门螺杆菌后建立AD样症状模型。酶联免疫吸附试验(ELISA)分析关键炎症因子的表达和血清免疫球蛋白E(IgE)水平。免疫组化染色分析聚丝蛋白（FLG）和菊甲蛋白（LOR）的表达。评价STAT1、STAT3、磷酸化STAT1(phospho-STAT1)、和磷酸化STAT3（磷酸化-STAT1）在皮肤病变中的表达水平使用蛋白质印迹。
结果：本研究表明，幽门螺杆菌阳性AD组（HP+AD+）表现出轻度皮肤病变，包括红斑,侵蚀,肿胀,和缩放，幽门螺杆菌阴性AD组（HP-AD+）。此外,HP+AD+显示血清中IgE水平较低，并下调血清中白细胞介素4和31（IL-4和IL-31）的表达。此外，与HP-AD相比，HPAD显示出更高的聚丝蛋白和loricrin表达。值得注意的是,H.pylori显著降低磷酸化STAT1和STAT3的量。
结论：幽门螺杆菌感染通过影响免疫反应中的炎症因子负调节炎症反应。修复有缺陷的表皮屏障功能。此外,幽门螺杆菌感染可以减少IL-31,从而减轻瘙痒。这些作用可能与JAK-STAT信号激活的抑制有关。
方法：用2,4-二硝基氯苯（DNCB）感染幽门螺杆菌后建立AD样症状模型。酶联免疫吸附试验(ELISA)分析关键炎症因子的表达和血清免疫球蛋白E(IgE)水平。免疫组化染色分析聚丝蛋白（FLG）和菊甲蛋白（LOR）的表达。评价STAT1、STAT3、磷酸化STAT1(phospho-STAT1)、和磷酸化STAT3（磷酸化-STAT1）在皮肤病变中的表达水平使用蛋白质印迹。
结果：本研究表明，幽门螺杆菌阳性AD组（HP+AD+）表现出轻度皮肤病变，包括红斑,侵蚀,肿胀,和缩放，幽门螺杆菌阴性AD组（HP-AD+）。此外,HP+AD+显示血清中IgE水平较低，并下调血清中白细胞介素4和31（IL-4和IL-31）的表达。此外，与HP-AD相比，HPAD显示出更高的聚丝蛋白和loricrin表达。值得注意的是,H.pylori显著降低磷酸化STAT1和STAT3的量。
结论：幽门螺杆菌感染通过影响免疫反应中的炎症因子负调节炎症反应。修复有缺陷的表皮屏障功能。此外,幽门螺杆菌感染可以减少IL-31,从而减轻瘙痒。这些作用可能与JAK-STAT信号激活的抑制有关。
