Respiratory syncytial virus (RSV) lower respiratory tract infection (LRTI) causes significant morbidity and mortality among young infants worldwide. It is currently widely accepted that neutrophil influx into the airways is a hallmark of the pathophysiology. However, the exact mechanism of neutrophil migration from the vasculature into the alveolar space in RSV LRTI has received little attention. Data shows that endothelial cells become activated upon RSV infection, driving a 'pro-adhesive state' for circulating neutrophils with upregulation of endothelial intercellular adhesion molecule-1 (ICAM-1). During RSV LRTI different subsets of immature and mature neutrophils are present in the bloodstream, that upregulate integrins lymphocyte-function associated antigen (LFA)-1 and macrophage (Mac)-1, serving as ICAM-1 ligands. An alveolar gradient of interleukin-8 may serve as a potent chemoattractant for circulating neutrophils. Neutrophils from lung aspirates of RSV-infected infants show further signs of inflammatory and migratory activation, while soluble endothelial cell adhesion molecules (sCAMs), such as sICAM-1, have become measurable in the systemic circulation. Whether these mechanisms are solely responsible for neutrophil migration into the alveolar space remains under debate. However, data indicate that the currently postulated neutrophil influx into the lungs should rather be regarded as a neutrophil efflux from the vasculature, involving substantial neutrophil-endothelial interactions. Molecular patterns of these interactions may be clinically useful to predict outcomes of RSV LRTI and deserve further study.

中文翻译：

---

呼吸道合胞病毒细支气管炎中的嗜中性粒细胞-内皮相互作用：尚未充分研究的方面，可预测疾病的严重程度。

呼吸道合胞病毒（RSV）下呼吸道感染（LRTI）在世界范围内的年轻婴儿中引起大量发病和死亡。当前，中性粒细胞流入气道是病理生理学的标志，这一点已被广泛接受。但是，嗜中性粒细胞从脉管系统迁移到RSV LRTI中的肺泡空间的确切机制很少受到关注。数据显示，内皮细胞在RSV感染后被激活，通过循环性内皮细胞间粘附分子1（ICAM-1）上调，驱动循环中性粒细胞处于“促粘附状态”。在RSV LRTI期间，血液中存在未成熟和成熟的中性粒细胞的不同子集，这些子集上调整合素淋巴细胞功能相关抗原（LFA）-1和巨噬细胞（Mac）-1，作为ICAM-1配体。白细胞介素8的肺泡梯度可作为循环中性粒细胞的有效化学引诱剂。来自RSV感染婴儿的肺吸出物的中性粒细胞显示出炎症和迁移活化的进一步迹象，而可溶性内皮细胞粘附分子（sCAMs），例如sICAM-1，已在系统循环中被测量。这些机制是否是中性粒细胞向肺泡空间迁移的唯一原因仍存在争议。但是，数据表明，目前假定的中性粒细胞流入肺应该被认为是来自脉管系统的中性粒细胞流出，涉及大量的中性粒细胞-内皮相互作用。这些相互作用的分子模式可能在临床上可用于预测RSV LRTI的预后，值得进一步研究。