铜绿假单胞菌( Pa )感染的慢性伤口的特点是疾病进展和死亡率增加。我们揭示了 Pf，一种由Pa产生的噬菌体，它可以延迟人类受试者和疾病动物模型中慢性感染伤口的愈合。有趣的是，Pf 对伤口闭合的损害与其对Pa发病机制的影响无关。相反，Pf 通过直接抑制 CXCL1 信号传导来阻碍角质形成细胞迁移，这对于伤口愈合至关重要。为了支持这些发现，一项对 36 名患有慢性Pa伤口感染的人类患者进行的前瞻性队列研究表明，与感染 Pf 阴性菌株的伤口相比，感染 Pf 阳性 Pa 菌株的伤口更容易变大。总之，这些数据表明 Pf 噬菌体通过直接操作哺乳动物细胞参与与Pa感染相关的伤口愈合延迟。这些发现表明 Pf 可能具有作为慢性伤口的生物标志物和治疗靶点的潜力。

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Chronic wounds infected by Pseudomonas aeruginosa (Pa) are characterized by disease progression and increased mortality. We reveal Pf, a bacteriophage produced by Pa that delays healing of chronically infected wounds in human subjects and animal models of disease. Interestingly, impairment of wound closure by Pf is independent of its effects on Pa pathogenesis. Rather, Pf impedes keratinocyte migration, which is essential for wound healing, through direct inhibition of CXCL1 signaling. In support of these findings, a prospective cohort study of 36 human patients with chronic Pa wound infections reveals that wounds infected with Pf-positive strains of Pa are more likely to progress in size compared with wounds infected with Pf-negative strains. Together, these data implicate Pf phage in the delayed wound healing associated with Pa infection through direct manipulation of mammalian cells. These findings suggest Pf may have potential as a biomarker and therapeutic target in chronic wounds.