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P38脂蛋白在穿透支原体黏附人尿道上皮细胞中的作用。

Role of P38 lipoprotein in Mycoplasma penetrans adhesion to human urothelial cells.

作者信息

Zhang Kaihua, Zou Weilu, Chen Yanming

机构信息

Department of Blood Transfusion, The Second Affiliated Hospital, University of South China, Hengyang, Hunan, 421001, China.

Department of Pain Rehabilitation, The Second Affiliated Hospital, University of South China, Hengyang, Hunan, 421001, China.

出版信息

BMC Microbiol. 2025 Aug 30;25(1):566. doi: 10.1186/s12866-025-04215-w.

Abstract

Mycoplasma penetrans, a bacterium detected in individuals seropositive for HIV and phylogenetically clustered with M. muris, may contribute to the progression of Acquired Immune Deficiency Syndrome (AIDS). Cellular adhesion is essential for Mycoplasma infection of host cells. M. penetrans exhibits the capacity to adhere to and invade human cells, precipitating diseases of the genital and urinary tracts. However, the proteinaceous mediators of its adhesion remain largely elusive. The P35 family lipoprotein, encoded by the mpl gene, is a prominent surface lipoprotein of M. penetrans. Here, we investigated the role of P38, a member of the P35 family, in the adhesion of M. penetrans to human urothelial cells (SV-HUC-1). We expressed and purified recombinant P38 (rP38) and confirmed its localization using Western blot. Adhesion assays, adhesion inhibition assays, and adhesion competition assays were performed to evaluate the adhesive properties of rP38 and M. penetrans. Our findings indicated that P38 localizes to the cell membrane of M. penetrans. Both rP38 and M. penetrans adhered to SV-HUC-1 cells, with optimal adhesion observed at 60 μg/mL for rP38 and 1 × 10⁷ CCU (Colony-Changing Units)/mL for M. penetrans. Anti-rP38 serum partially inhibited M. penetrans adhesion to SV-HUC-1 cells, and rP38 competed with M. penetrans for binding to SV-HUC-1 cells. These results suggest that P38 may function as an adhesin of M. penetrans, providing insights into its pathogenic mechanisms.

摘要

穿透支原体是一种在HIV血清反应阳性个体中检测到的细菌,在系统发育上与鼠支原体聚类,可能会促进获得性免疫缺陷综合征(AIDS)的发展。细胞黏附对于支原体感染宿主细胞至关重要。穿透支原体具有黏附和侵入人类细胞的能力,可引发泌尿生殖道疾病。然而,其黏附的蛋白质介导因子在很大程度上仍不明确。由mpl基因编码的P35家族脂蛋白是穿透支原体的一种主要表面脂蛋白。在此,我们研究了P35家族成员P38在穿透支原体与人尿路上皮细胞(SV-HUC-1)黏附中的作用。我们表达并纯化了重组P38(rP38),并通过蛋白质免疫印迹法确认了其定位。进行了黏附试验、黏附抑制试验和黏附竞争试验,以评估rP38和穿透支原体的黏附特性。我们的研究结果表明,P38定位于穿透支原体的细胞膜。rP38和穿透支原体均能黏附于SV-HUC-1细胞,rP38在60μg/mL时观察到最佳黏附效果,穿透支原体在1×10⁷CCU(菌落形成单位)/mL时观察到最佳黏附效果。抗rP38血清部分抑制了穿透支原体对SV-HUC-1细胞的黏附,并且rP38与穿透支原体竞争结合SV-HUC-1细胞。这些结果表明,P38可能作为穿透支原体的一种黏附素发挥作用,为其致病机制提供了见解。

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