白细胞介素-22 可减轻急性呼吸窘迫综合征（ARDS）。
Interleukin-22 mitigates acute respiratory distress syndrome (ARDS).
机构信息
Department of Surgery, Tulane University School of Medicine, New Orleans, LA, United States of America.
Tulane University School of Medicine, Center for Translational Research in Infection and Inflammation, New Orleans, LA, United States of America.
出版信息
PLoS One. 2021 Oct 1;16(10):e0254985. doi: 10.1371/journal.pone.0254985. eCollection 2021.
BACKGROUND
The goal of this study was to determine if IL-22:Fc would Acute Respiratory Distress Syndrome (ARDS).
SUMMARY BACKGROUND DATA
No therapies exist for ARDS and treatment is purely supportive. Interleukin-22 (IL-22) plays an integral component in recovery of the lung from infection. IL-22:Fc is a recombinant protein with a human FC immunoglobulin that increases the half-life of IL-22.
STUDY DESIGN
ARDS was induced in C57BL/6 mice with intra-tracheal lipopolysaccharide (LPS) at a dose of 33.3 or 100 ug. In the low-dose LPS group (LDG), IL-22:FC was administered via tail vein injection at 30 minutes (n = 9) and compared to sham (n = 9). In the high-dose LPS group (HDG), IL-22:FC was administered (n = 11) then compared to sham (n = 8). Euthanasia occurred after bronchioalveolar lavage (BAL) on post-injury day 4.
RESULTS
In the LDG, IL-22:FC resulted in decreased protein leak (0.15 vs. 0.25 ug/uL, p = 0.02). BAL protein in animals receiving IL-22:Fc in the HDG was not different. For the HDG, animals receiving IL-22:Fc had lower BAL cell counts (539,636 vs 3,147,556 cells/uL, p = 0.02). For the HDG, IL-6 (110.6 vs. 527.1 pg/mL, p = 0.04), TNF-α (5.87 vs. 25.41 pg/mL, p = 0.04), and G-CSF (95.14 vs. 659.6, p = 0.01) levels were lower in the BAL fluid of IL-22:Fc treated animals compared to sham.
CONCLUSIONS
IL-22:Fc decreases lung inflammation and lung capillary leak in ARDS. IL-22:Fc may be a novel therapy for ARDS.
背景
本研究旨在确定 IL-22：Fc 是否会导致急性呼吸窘迫综合征（ARDS）。
背景数据概要
目前尚无 ARDS 的治疗方法，治疗仅为支持性治疗。白细胞介素 22（IL-22）在感染后肺部恢复中发挥着重要作用。IL-22：Fc 是一种重组蛋白，具有增加 IL-22 半衰期的人 FC 免疫球蛋白。
研究设计
用气管内脂多糖（LPS）以 33.3 或 100ug 的剂量诱导 C57BL/6 小鼠发生 ARDS。在低剂量 LPS 组（LDG）中，IL-22：Fc 在 30 分钟时通过尾静脉注射给药（n = 9），并与假手术组（n = 9）进行比较。在高剂量 LPS 组（HDG）中，给予 IL-22：Fc（n = 11），然后与假手术组（n = 8）进行比较。在损伤后第 4 天进行支气管肺泡灌洗（BAL）后进行安乐死。
结果
在 LDG 中，IL-22：Fc 导致蛋白漏出减少（0.15 与 0.25ug/uL，p = 0.02）。在 HDG 中接受 IL-22：Fc 的动物的 BAL 蛋白无差异。对于 HDG，接受 IL-22：Fc 的动物的 BAL 细胞计数较低（539,636 与 3,147,556 细胞/uL，p = 0.02）。对于 HDG，IL-6（110.6 与 527.1pg/mL，p = 0.04），TNF-α（5.87 与 25.41pg/mL，p = 0.04）和 G-CSF（95.14 与 659.6，p = 0.01）在 BAL 液中的水平低于假手术组。
结论
IL-22：Fc 可减少 ARDS 中的肺部炎症和肺毛细血管漏。IL-22：Fc 可能是 ARDS 的一种新疗法。
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