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对……中氧化应激的反应

Response to Oxidative Stress in .

作者信息

Ruiz-Baca Estela, Adame-Soto Pablo Jaciel, Alba-Fierro Carlos Antonio, Martínez-Rocha Ana Lilia, Pérez-Torres Armando, López-Rodríguez Angélica, Romo-Lozano Yolanda

机构信息

Facultad de Ciencias Químicas, Universidad Juárez del Estado de Durango, Av. Veterinaria S/N, Durango C.P. 34120, Mexico.

Departamento de Biología, División de Ciencias Naturales y Exactas, Universidad de Guanajuato, Guanajuato C.P. 36050, Mexico.

出版信息

J Fungi (Basel). 2025 Jun 10;11(6):440. doi: 10.3390/jof11060440.

Abstract

Oxidative stress is key in immune defense against fungal infections, such as those caused by , the dimorphic fungus responsible for sporotrichosis. Phagocytic cells utilize oxidative stress as a crucial mechanism to control pathogen spread. During infection, phagocytic cells recognize pathogen-associated molecular patterns (PAMPs) on their surface through conserved transmembrane or soluble receptors, known as pattern recognition receptors (PRRs). This recognition triggers a cascade of immune responses, including the generation reactive oxygen species (ROS) essential for pathogen elimination. However, has developed sophisticated mechanisms to evade and counteract this response, contributing to its persistence in the host. These mechanisms include the production of antioxidant enzymes, alterations to its cell wall (CW), and the production of melanin, which helps neutralize oxidative stress. In addition, modulates the production of other proteins, such as moonlighting proteins, suggested to have roles in immune evasion and stress response, helping its survival in the host. These strategies, along with the modulation of gene expression, allow the fungus to survive and persist inside the immune system's hostile environment, facilitating the progression of the infection. Understanding these interactions between phagocytic cells and is key to developing more effective therapeutic strategies to combat sporotrichosis.

摘要

氧化应激是抵抗真菌感染(如由引起孢子丝菌病的双态真菌所引发的感染)的免疫防御中的关键因素。吞噬细胞利用氧化应激作为控制病原体传播的关键机制。在感染期间,吞噬细胞通过保守的跨膜或可溶性受体(称为模式识别受体,PRRs)识别其表面的病原体相关分子模式(PAMPs)。这种识别触发一系列免疫反应,包括产生对消除病原体至关重要的活性氧(ROS)。然而,已经发展出复杂的机制来逃避和对抗这种反应,这有助于其在宿主体内持续存在。这些机制包括抗氧化酶的产生、其细胞壁(CW)的改变以及黑色素的产生,黑色素有助于中和氧化应激。此外,还调节其他蛋白质的产生,如兼性蛋白,提示其在免疫逃避和应激反应中发挥作用,有助于其在宿主体内存活。这些策略,连同基因表达的调节,使真菌能够在免疫系统的恶劣环境中存活和持续存在,促进感染的进展。了解吞噬细胞与之间的这些相互作用是开发更有效的治疗孢子丝菌病策略的关键。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f344/12193860/3ad3e0c224c3/jof-11-00440-g001.jpg

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