Department of Emergency, The Affiliated Huai'an Hospital of Xuzhou Medical University and The Second People's Hospital of Huai'an, No. 62, Huaihai Road (S.), Huai'an 223002, China.
Department of Emergency, Siyang Hospital of Traditiona Chinese Medicine, No. 15, North Jiefang Road, Siyang 223700, Jiangsu Province, China.
Gene. 2023 Aug 20;878:147575. doi: 10.1016/j.gene.2023.147575. Epub 2023 Jun 20.
In addition to oxidative damage, sepsis can cause multiple organ dysfunction and poses a life-threatening threat. In addition to severe tissue damage, hypotension, and multiple organ failure, sepsis can cause high morbidity and mortality. It is the lungs that are most vulnerable in abdominal sepsis, with impaired oxygen and nutrient exchange occurring in the pulmonary microcirculation. However, the etiology of sepsis and the link between sepsis and lung injury has not been elucidated. In this work, by exploring the data from the GEO and CTD database, a gene association study was conducted to determine whether sepsis-induced lung injury is caused by BPA. Further analysis demonstrated that MMP9, CEBPA, CYP1B1, CTSD, FKBP5, DGAT2, HP, TIMP2, ARG1 and MGST1 may play an important role in sepsis-induced lung injury. Finally, the single-cell RNA sequence demonstrated that CEBPA is mainly enriched in lung epithelial cells and epithelial cells, whereas CYP1B1 is closely related to basal cells, macrophages, and interstitial cells. In order to maintain lung function, epithelial and alveolar macrophages as well as other lung cells are important. When the lung epithelium is activated for a prolonged period of time, barrier function may be compromised and tissue damage may result, aggravating the lung injury. By using the animal model, we successfully simulated the model of sepsis lung injury. The HE staining demonstrated the rats with BPA-treated septic lung injury showed more alveolar structure to be disordered, pulmonary interstitial edema to be evident, and red blood cells as well as inflammatory cells. For PCR assay, the results demonstrated that the expression level of CEBPA is higher in the lung samples with sepsis compared with the normal samples of the lung. In order to evaluate the expression level of CEBPA and CYP1B1 in lung tissue, we then performed the PCR assay. For CYP1B1, the results demonstrated that the expression level of CYP1B1 in lung samples with sepsis is lower than in normal lung samples. In total, BPA may be a potential contributing factor to sepsis-induced lung injury.
除了氧化损伤，脓毒症还会导致多器官功能障碍，对生命构成威胁。除了严重的组织损伤、低血压和多器官衰竭，脓毒症还会导致高发病率和死亡率。在腹部脓毒症中，肺部最容易受到影响，肺微循环中的氧气和营养交换受到损害。然而，脓毒症的病因以及脓毒症与肺损伤之间的联系尚未阐明。在这项工作中，通过探索 GEO 和 CTD 数据库中的数据，进行了基因关联研究，以确定 BPA 是否会导致脓毒症引起的肺损伤。进一步的分析表明，MMP9、CEBPA、CYP1B1、CTSD、FKBP5、DGAT2、HP、TIMP2、ARG1 和 MGST1 可能在脓毒症引起的肺损伤中发挥重要作用。最后，单细胞 RNA 序列表明，CEBPA 主要在肺上皮细胞和上皮细胞中富集，而 CYP1B1 与基底细胞、巨噬细胞和间质细胞密切相关。为了维持肺功能，上皮细胞和肺泡巨噬细胞以及其他肺细胞是重要的。当肺上皮细胞长时间被激活时，屏障功能可能会受损，导致组织损伤，从而加重肺损伤。通过使用动物模型，我们成功模拟了脓毒症肺损伤模型。HE 染色显示，BPA 处理的脓毒症肺损伤大鼠的肺泡结构更加紊乱，肺间质水肿明显，红细胞和炎症细胞增多。对于 PCR 检测，结果表明脓毒症肺组织中 CEBPA 的表达水平高于正常肺组织。为了评估肺组织中 CEBPA 和 CYP1B1 的表达水平，我们随后进行了 PCR 检测。对于 CYP1B1，结果表明脓毒症肺组织中 CYP1B1 的表达水平低于正常肺组织。总之，BPA 可能是脓毒症引起肺损伤的一个潜在因素。
