PRRSV-induced inflammation in pulmonary intravascular macrophages (PIMs) and pulmonary alveolar macrophages (PAMs) contributes to endothelial barrier function injury

炎症 势垒函数 封堵器 生物 免疫学 肿瘤坏死因子α 猪繁殖与呼吸综合征病毒 紧密连接 医学 细胞生物学 病毒 内科学
作者
Sun Zheng,Xiaolei Chen,Jiao Liu,Yingbin Du,Chenrui Duan,Shaobo Xiao,Yanrong Zhou,Liurong Fang
出处
期刊:Veterinary Microbiology [Elsevier]
卷期号:281: 109730-109730 被引量:2
标识
DOI:10.1016/j.vetmic.2023.109730
摘要

Porcine reproductive and respiratory syndrome (PRRS) is a severe infectious disease currently devasting the global pig industry. PRRS is characterized by intense inflammation and severe damage to the alveolar-capillary barrier. Therefore, it is crucial to uncover the underlying mechanism by which the PRRS virus (PRRSV) induces inflammatory responses and barrier function damage. In addition to porcine alveolar macrophages (PAMs), the primary target cells of PRRSV infection in vivo, pulmonary intravascular macrophages (PIMs) are also susceptible to PRRSV infection. However, the poor isolation efficiency limits the study of PRRSV infection in PIMs. In this study, we optimized the isolation method to obtain PIMs with higher purity and yield and demonstrated that PRRSV's infection kinetics in PIMs were similar to those in PAMs. Notably, PIMs exhibited a more acute inflammation process during PRRSV infection than PAMs, as evidenced by the earlier upregulation and higher levels of pro-inflammatory cytokines, including TNF-α and IL-1β. More acute endothelial barrier disfunction upon PRRSV infection was also observed in PIMs compared to in PAMs. Mechanistically, PRRSV-induced TNF-α and IL-1β could cause endothelial barrier disfunction by dysregulating tight junction proteins, including claudin 1 (CLDN1), claudin 8 (CLDN8) and occludin (OCLN). Our findings revealed the crucial and novel roles of PIMs in facilitating the progression of inflammatory responses and endothelial barrier injury and provided new insights into the mechanisms of PRRSV's induction of interstitial pneumonia.
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