Sztandera-Tymoczek Monika, Wdowiak-Wróbel Sylwia, Świderska Urszula, Palusińska-Szysz Marta, Szuster-Ciesielska Agnieszka
Department of Virology and Immunology, Institute of Biological Sciences, Maria Curie-Skłodowska University, Lublin, Poland.
Department of Genetics and Microbiology, Institute of Biological Sciences, Maria Curie-Skłodowska University, Lublin, Poland.
J Inflamm Res. 2025 Jan 25;18:1107-1125. doi: 10.2147/JIR.S497219. eCollection 2025.
Allergic diseases have escalated to epidemic levels worldwide, impacting nearly 30% of the global population. Fungi are a significant source of allergens responsible for up to 6% of respiratory diseases in the general population. However, the specific cause of respiratory allergies often remains unidentified. This study aimed to investigate the potential of two common rust fungi, and , to trigger a proinflammatory response in vitro models representing the upper and lower respiratory tract.
The BEAS-2B and A549 cell lines simulated upper and lower respiratory endothelial cells. The cytotoxicity of fungal extracts was evaluated using MTT and flow cytometry assays. Cell reactive oxygen species (ROS) production was measured via flow cytometry, while ELISA tests quantified the production of proinflammatory cytokines. Immunofluorescence techniques were employed to assess cell integrity markers.
Extracts from and significantly stimulated the production of proinflammatory cytokines IL-1β and GM-CSF in both cell lines, all of which are associated with the development of allergic responses. The increase in these cytokines and the elevated ROS production were linked to the disruption of epithelial cell junctions.
The findings suggest the potential of and extracts to collectively disrupt the epithelial barrier in the upper and lower respiratory tract by inducing proinflammatory cytokines and the production of reactive oxygen species and metalloproteinases. Although none of the above parameters was spectacularly high, all of them together could cause a decrease in the presence of tight junction proteins, such as E-cadherin and occludin, in epithelial cells.
过敏性疾病在全球范围内已升级至流行水平，影响了近30%的全球人口。真菌是过敏原的重要来源，在普通人群中导致高达6%的呼吸道疾病。然而，呼吸道过敏的具体原因往往仍不明确。本研究旨在调查两种常见锈菌引发上呼吸道和下呼吸道体外模型促炎反应的潜力。
BEAS-2B和A549细胞系模拟上呼吸道和下呼吸道内皮细胞。使用MTT和流式细胞术检测评估真菌提取物的细胞毒性。通过流式细胞术测量细胞活性氧（ROS）的产生，而ELISA试验定量促炎细胞因子的产生。采用免疫荧光技术评估细胞完整性标志物。
两种锈菌的提取物均显著刺激了两种细胞系中促炎细胞因子IL-1β和GM-CSF的产生，所有这些都与过敏反应的发展有关。这些细胞因子的增加和ROS产生的升高与上皮细胞连接的破坏有关。
研究结果表明，两种锈菌提取物有可能通过诱导促炎细胞因子、活性氧的产生和金属蛋白酶，共同破坏上呼吸道和下呼吸道的上皮屏障。尽管上述参数均未显著升高，但所有这些因素共同作用可能导致上皮细胞中紧密连接蛋白（如E-钙黏蛋白和闭合蛋白）的含量降低。
