Department of Pathogenobiology, Jilin University Mycology Research Center, Key Laboratory of Zoonosis Research, Ministry of Education, College of Basic Medical Sciences, Jilin University , Changchun, China.
Department of Dermatology, First Affiliated Hospital of Dalian Medical University , Dalian, China.
Microbiol Spectr. 2024 Jan 11;12(1):e0269923. doi: 10.1128/spectrum.02699-23. Epub 2023 Nov 29.
can infect immunocompromised individuals and cause chronic and fatal invasive fungal infections. A better understanding of the molecular mechanisms of -host interactions may provide new references for disease treatment. In this study, we demonstrated that the TRAF3 gene plays an important role in the early infection of by regulating the resistance of lung epithelial cells to . Macrophages are the most abundant innate immune cells in the alveoli; however, few studies have reported on the interactions between lung epithelial cells and macrophages in response to invasion. In our study, it was demonstrated that the TRAF3 gene reduces migration to macrophages and cytokine production by negatively regulating lung epithelial cell adhesion and internalization of spores. Together, our results provide new insights into lung epithelial cell-macrophage interactions during infection.
可以感染免疫功能低下的个体，并导致慢性和致命的侵袭性真菌感染。更好地了解宿主相互作用的分子机制可能为疾病治疗提供新的参考。在这项研究中，我们表明 TRAF3 基因在通过调节肺上皮细胞对的抗性来控制的早期感染中发挥重要作用。巨噬细胞是肺泡中最丰富的先天免疫细胞;然而，很少有研究报道肺上皮细胞与巨噬细胞在应对侵袭时的相互作用。在我们的研究中，证明 TRAF3 基因通过负调控肺上皮细胞对孢子的黏附和内化，减少向巨噬细胞的迁移和细胞因子的产生。总之，我们的研究结果为研究期间肺上皮细胞与巨噬细胞的相互作用提供了新的见解。
