A corollary study to substantiate the therapeutic role of receptor from Shigella flexneri in mitigating the sperm immobilization factor-mediated negative influences on mouse spermatozoa: a molecular mimicry-based approach.

IF 2.1
Thomson Soni, Ishwerpreet Kaur Jawanda, Seema Kumari, Vijay Prabha
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Abstract

Context Sperm immobilization factor (SIF) isolated from Staphylococcus aureus has been implicated earlier in the laboratory in infertility due to its negative impact on sperm function. Moreover, SIF was found to bind not only to human and mouse spermatozoa but also to several bacteria. Among the array of bacteria, we selected Shigella flexneri to investigate if it shares antigenic determinants with spermatozoa. Aim The study aimed to delineate receptors from S. flexneri that imitate the sperm receptor in binding SIF, to assess its therapeutic role in SIF-mediated sperm impairment. Methods Sperm immobilization binding receptor (SBR) from S. flexneri (SF-SBR) was isolated via ultrasonication and 4M NaCl treatment, purified via chromatography and its molecular weight was estimated. The ability of SF-SBR to counteract SIF-induced sperm impairment was assessed in vitro . Further analysis included isothermal titration calorimetry and fourier-transform infrared spectroscopy to quantify the interaction of SIF and SF-SBR. Key results SF-SBR ameliorated the sperm parameters adversely affected by SIF. It also interfered with the binding of fluorescein isothiocyanate-labelled SIF to spermatozoa and bacteria. The SIF and SF-SBR interaction showed favourable thermodynamics with an entropy of 28.12J/molK and free energy of -18.48kJ/mol, supporting the concept of mimicry. Conclusions The study confirmed that SF-SBR shares an epitope with the receptor on mouse spermatozoa, affirming the presence of molecular mimicry between spermatozoa and S. flexneri . Implications These findings indicate that SF-SBR can potentially be used to counteract the effects of SIF on spermatozoa, hinting at novel therapeutic approaches for treating infertility caused by microbial sperm immobilization factors.

一项基于分子模拟的研究证实了福氏志贺氏菌受体在减轻精子固定因子介导的对小鼠精子的负面影响中的治疗作用。
背景 从金黄色葡萄球菌(Staphylococcus aureus)中分离出的精子固定因子(SIF)因其对精子功能的负面影响,早先在实验室中被认为与不育症有关。此外,研究发现 SIF 不仅能与人类和小鼠精子结合,还能与多种细菌结合。在这一系列细菌中,我们选择了柔性志贺氏菌(Shigella flexneri)来研究它是否与精子具有相同的抗原决定簇。目的 本研究旨在确定柔性志贺氏菌中可模仿精子受体与 SIF 结合的受体,以评估其在 SIF 介导的精子损伤中的治疗作用。方法 通过超声波处理和 4M NaCl 处理,分离出柔红细胞虫的精子固定结合受体(SBR),并通过色谱法纯化和估算其分子量。在体外评估了 SF-SBR 抵消 SIF 诱导的精子损伤的能力。进一步的分析包括等温滴定量热法和傅立叶变换红外光谱法,以量化 SIF 和 SF-SBR 的相互作用。主要结果 SF-SBR 可改善受 SIF 负面影响的精子参数。它还干扰了异硫氰酸荧光素标记的 SIF 与精子和细菌的结合。SIF 和 SF-SBR 的相互作用显示出有利的热力学性质,熵为 28.12J/molK ,自由能为 -18.48kJ/mol,支持拟态概念。结论 该研究证实,SF-SBR 与小鼠精子上的受体具有共同的表位,从而肯定了精子与柔直杆菌之间存在分子拟态作用。意义 这些研究结果表明,SF-SBR 有可能用于抵消 SIF 对精子的影响,为治疗由微生物精子固定因子引起的不育症提供了新的治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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