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脂多糖诱导的气道炎症和杯状细胞增生的消退与白细胞介素-18无关。

Resolution of LPS-induced airway inflammation and goblet cell hyperplasia is independent of IL-18.

作者信息

Harris J Foster, Aden Jay, Lyons C Rick, Tesfaigzi Yohannes

机构信息

Lovelace Respiratory Research Institute, Albuquerque, NM, USA.

出版信息

Respir Res. 2007 Mar 12;8(1):24. doi: 10.1186/1465-9921-8-24.

DOI:10.1186/1465-9921-8-24
PMID:17352829
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1828726/
Abstract

BACKGROUND

The resolution of inflammatory responses in the lung has not been described in detail and the role of specific cytokines influencing the resolution process is largely unknown.

METHODS

The present study was designed to describe the resolution of inflammation from 3 h through 90 d following an acute injury by a single intratracheal instillation of F344/N rats with LPS. We documented the inflammatory cell types and cytokines found in the bronchoalveolar lavage fluid (BALF), and epithelial changes in the axial airway and investigated whether IL-18 may play a role in the resolution process by reducing its levels with anti-IL-18 antibodies.

RESULTS

Three major stages of inflammation and resolution were observed in the BALF during the resolution. The first stage was characterized by PMNs that increased over 3 h to 1 d and decreased to background levels by d 6-8. The second stage of inflammation was characterized by macrophage influx reaching maximum numbers at d 6 and decreasing to background levels by d 40. A third stage of inflammation was observed for lymphocytes which were elevated over d 3-6. Interestingly, IL-18 and IL-9 levels in the BALF showed a cyclic pattern with peak levels at d 4, 8, and 16 while decreasing to background levels at d 1-2, 6, and 12. Depletion of IL-18 caused decreased PMN numbers at d 2, but no changes in inflammatory cell number or type at later time points.

CONCLUSION

These data suggest that IL-18 plays a role in enhancing the LPS-induced neutrophilic inflammation of the lung, but does not affect the resolution of inflammation.

摘要

背景

肺部炎症反应的消退尚未得到详细描述，影响消退过程的特定细胞因子的作用在很大程度上也不清楚。

方法

本研究旨在描述单次气管内滴注脂多糖（LPS）对F344/N大鼠造成急性损伤后3小时至90天内炎症的消退情况。我们记录了支气管肺泡灌洗液（BALF）中发现的炎症细胞类型和细胞因子，以及轴向气道的上皮变化，并通过用抗IL-18抗体降低其水平来研究IL-18是否可能在消退过程中发挥作用。

结果

在消退过程中，BALF中观察到炎症和消退的三个主要阶段。第一阶段的特征是中性粒细胞在3小时至1天内增加，并在第6 - 8天降至背景水平。炎症的第二阶段的特征是巨噬细胞在第6天大量涌入，并在第40天降至背景水平。观察到炎症的第三阶段是淋巴细胞在第3 - 6天升高。有趣的是，BALF中的IL-18和IL-9水平呈现周期性模式，在第4、8和16天达到峰值水平，而在第1 - 2、6和12天降至背景水平。IL-18的耗竭导致第2天中性粒细胞数量减少，但在后期时间点炎症细胞数量或类型没有变化。

结论

这些数据表明，IL-18在增强LPS诱导的肺部嗜中性炎症中起作用，但不影响炎症的消退。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4189/1828726/05ff10e9ce07/1465-9921-8-24-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4189/1828726/a7970026a178/1465-9921-8-24-1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4189/1828726/05ff10e9ce07/1465-9921-8-24-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4189/1828726/a7970026a178/1465-9921-8-24-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4189/1828726/0cdec34971c2/1465-9921-8-24-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4189/1828726/dc9ce50dc0b2/1465-9921-8-24-3.jpg
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J Clin Invest. 2006 Feb;116(2):309-21. doi: 10.1172/JCI25167.
2
Roles of apoptosis in airway epithelia.细胞凋亡在气道上皮中的作用。
Am J Respir Cell Mol Biol. 2006 May;34(5):537-47. doi: 10.1165/rcmb.2006-0014OC. Epub 2006 Jan 26.
3
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4
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5
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