Helicobacter pylori infection attenuates 2,4-dinitrochlorobenzene-induced atopic dermatitis-like skin lesions in C57/BL6 mice.

IF 2.6 4区医学 Q2 ALLERGY Allergy Asthma and Clinical Immunology Pub Date : 2023-11-17 DOI:10.1186/s13223-023-00851-x

Shuxian Wang, Xiaokang Wang, Jiaqi Liu, Yaqian Li, Minghui Sun, Guoqiang Zhu, Xiaofang Zhu

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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.

Conclusion: 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.

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幽门螺杆菌感染可减轻C57/BL6小鼠2,4-二硝基氯苯诱导的特应性皮炎样皮肤病变。

背景:虽然大量研究表明幽门螺杆菌(h.p ylori)感染与过敏呈负相关，但关于幽门螺杆菌感染与特应性皮炎(AD)关系的研究有限。本研究旨在探讨幽门螺杆菌感染对AD小鼠模型的影响，并确定与2型免疫、皮肤屏障缺陷和瘙痒相关的潜在机制。方法:采用2,4-二硝基氯苯(DNCB)建立胃幽门螺旋杆菌感染后ad样症状模型。采用酶联免疫吸附试验(ELISA)分析各组关键炎症因子表达及血清免疫球蛋白E (IgE)水平。免疫组化染色分析聚丝蛋白(FLG)和loricrin (LOR)的表达。western blot检测皮肤病变组织中STAT1、STAT3、磷酸化STAT1 (phospho-STAT1)和磷酸化STAT3 (phospho-STAT1)的表达水平。结果:本研究显示，幽门螺杆菌阳性AD组(HP+AD+)的皮肤病变较幽门螺杆菌阴性AD组(HP-AD+)轻微，包括红斑、糜烂、肿胀和结垢。此外，HP+AD+患者血清中IgE水平降低，血清中白细胞介素4和31 (IL-4和IL-31)表达下调。HP+AD+比HP-AD+表达更高的聚丝蛋白和loricrin。值得注意的是，幽门螺杆菌显著降低了STAT1和STAT3的磷酸化量。结论:幽门螺杆菌感染通过影响免疫反应中的炎性因子负性调节炎症反应，修复表皮屏障功能缺陷。此外，幽门螺杆菌感染可降低IL-31，从而减轻瘙痒。这些作用可能与抑制JAK-STAT信号激活有关。

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来源期刊

Allergy Asthma and Clinical Immunology ALLERGY-IMMUNOLOGY

CiteScore

4.30

自引率

3.70%

发文量

审稿时长

12 weeks

期刊介绍： Allergy, Asthma & Clinical Immunology (AACI), the official journal of the Canadian Society of Allergy and Clinical Immunology (CSACI), is an open access journal that encompasses all aspects of diagnosis, epidemiology, prevention and treatment of allergic and immunologic disease. By offering a high-visibility forum for new insights and discussions, AACI provides a platform for the dissemination of allergy and clinical immunology research and reviews amongst allergists, pulmonologists, immunologists and other physicians, healthcare workers, medical students and the public worldwide. AACI reports on basic research and clinically applied studies in the following areas and other related topics: asthma and occupational lung disease, rhinoconjunctivitis and rhinosinusitis, drug hypersensitivity, allergic skin diseases, urticaria and angioedema, venom hypersensitivity, anaphylaxis and food allergy, immunotherapy, immune modulators and biologics, immune deficiency and autoimmunity, T cell and B cell functions, regulatory T cells, natural killer cells, mast cell and eosinophil functions, complement abnormalities.