由于猪繁殖和呼吸综合症病毒（PRRSV）感染引起的细胞和免疫事件的改变与肺的发病机制有关。PRRSV还会导致雌性生殖功能障碍和持续感染，这可能会传播到胎儿、死胎和后代。本研究在初级猪腺体内膜细胞（PGE）中检查对PRRSV类型1或类型2感染的细胞和先天免疫反应的变化，包括PRRSV介导物的表达、Toll样受体（TLRs）和细胞因子mRNA表达以及细胞因子分泌。细胞感染可通过细胞病理性效应（CPE）、PRRSV核衣壳蛋白和病毒核酸的检测在感染后2天即可观察到，并持续到6天后。在类型2感染中观察到更高比例的CPE和PRRSV阳性细胞。PRRSV介导蛋白CD151、CD163、唾液酸粘附素（Sn）、整合素和中间纤维蛋白在类型1和类型2感染后上调。CD151、CD163和Sn通过类型2感染上调。在PRRSV的两种类型中，TLR1和TLR6的mRNA表达上调。然而，TLR3通过类型1上调，但TLR4和TLR8的mRNA和蛋白只有类型2感染后下调。白细胞介素（IL）-1β、IL-6和肿瘤坏死因子（TNF）-α通过类型2上调，但IL-8通过类型1上调。PRRSV类型1和2都会刺激IL-6但抑制TNF-α分泌。此外，只有类型2会抑制IL-1β分泌。这些发现揭示了PRRSV感染在内膜中的重要机制，并与病毒持续感染相关。版权所有：© 2023 Lothong等人。本文是根据知识共享署名许可发布的开放获取文章，它允许在任何媒介中无限制使用、分发和复制，前提是保持原始作者和来源的署名。

Modification of cellular and immunological events due to porcine reproductive and respiratory syndrome virus (PRRSV) infection is associated with pathogenesis in lungs. PRRSV also causes female reproductive dysfunction and persistent infection which can spread to fetus, stillbirth, and offspring. In this study, changes in cellular and innate immune responses to PRRSV type 1 or type 2 infection, including expression of PRRSV mediators, mRNA expression of Toll-like receptors (TLRs) and cytokine, and cytokine secretion, were examined in primary porcine glandular endometrial cells (PGE). Cell infectivity as observed by cytopathic effect (CPE), PRRSV nucleocapsid proteins, and viral nucleic acids was detected as early as two days post-infection (2 dpi) and persisted until 6 dpi. A higher percentage of CPE and PRRSV-positive cells were observed in type 2 infections. PRRSV mediator proteins, CD151, CD163, sialoadhesin (Sn), integrin and vimentin, were upregulated following type 1 and type 2 infection. CD151, CD163 and Sn were upregulated by type 2. In both PRRSV types, mRNA expression of TLR1 and TLR6 was upregulated. However, TLR3 was upregulated by type 1, but TLR4 and TLR8 mRNA and protein were downregulated by type 2 only. Interleukin (IL)-1β, IL-6 and tumor necrotic factor (TNF)-α were upregulated by type 2, but IL-8 was upregulated by type 1. Both PRRSV type 1 and 2 stimulated IL-6 but suppressed TNF-α secretion. In addition, IL-1β secretion was suppressed only by type 2. These findings reveal an important mechanism underlying the strategy of PRRSV infection in the endometrium and associated with the viral persistence.Copyright: © 2023 Lothong et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.