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针对实验性重症哮喘和急性肺损伤中的常见炎症介质

Targeting Common Inflammatory Mediators in Experimental Severe Asthma and Acute Lung Injury.

作者信息

Vicovan Andrei Gheorghe, Petrescu Diana Cezarina, Cretu Aurelia, Ghiciuc Cristina Mihaela, Constantinescu Daniela, Iftimi Elena, Strugariu Georgiana, Ancuta Codrina Mihaela, Caratașu Cezar-Cătălin, Solcan Carmen, Stafie Celina Silvia

机构信息

Department of Morpho-Functional Sciences II-Pharmacology and Clinical Pharmacology, Faculty of Medicine, Grigore T. Popa University of Medicine and Pharmacy of Iasi, 16 Universitatii Street, 700115 Iasi, Romania.

"Saint Mary" Emergency Children Hospital, 700887 Iasi, Romania.

出版信息

Pharmaceuticals (Basel). 2024 Mar 5;17(3):338. doi: 10.3390/ph17030338.

DOI:10.3390/ph17030338
PMID:38543124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10974991/
Abstract

Neutrophils, known to be mobilized and activated in high amounts through Il-17 stimulation, are a key factor for clinical manifestation and imbalance of redox systems favoring a dominant oxidative state in both severe asthma and acute lung injury (f). The aim of this study was to evaluate in mice, the effect of Secukinumab (SECU) in a model of ovalbumin-induced asthma exacerbated with LPS administration to induce ALI, compared to dexamethasone (DEXA), already known for its benefit in both asthma and ALI. Results on cytokine levels for specific Th1, Th2 and Th17 revealed an interplay of immune responses. For Th1 effector cytokines in BALF, DEXA treatment increased TNF-α levels, but TNF-α was not modified by SECU; DEXA and SECU significantly decreased IFN-γ and IL-6 levels. For typical Th2 cytokines, DEXA significantly increased Il-4, Il-5 and Il-13 levels, while SECU significantly inhibited Il-5 levels. Both SECU and DEXA significantly decreased Il-17 levels. Cytokine level changes in lung tissue homogenate were partly similar to BALF cytokines. Conclusion: in addition to DEXA, SECU possesses the ability to modulate inflammatory cytokine release and to decrease Th17 responses in ALI overlapped on exacerbated asthma in mice.

摘要

已知中性粒细胞可通过白细胞介素-17刺激大量动员和激活，在严重哮喘和急性肺损伤中，中性粒细胞是临床表现和氧化还原系统失衡的关键因素，这种失衡有利于主导氧化状态（f）。本研究的目的是在小鼠中评估司库奇尤单抗（SECU）在卵清蛋白诱导的哮喘模型中（通过给予脂多糖诱导急性肺损伤使其恶化）的效果，并与地塞米松（DEXA）进行比较，地塞米松在哮喘和急性肺损伤中均有益处，这已为人所知。特定Th1、Th2和Th17细胞因子水平的结果揭示了免疫反应的相互作用。对于支气管肺泡灌洗液（BALF）中的Th1效应细胞因子，地塞米松治疗可提高肿瘤坏死因子-α（TNF-α）水平，但司库奇尤单抗未改变TNF-α水平；地塞米松和司库奇尤单抗均显著降低干扰素-γ（IFN-γ）和白细胞介素-6（IL-6）水平。对于典型的Th2细胞因子，地塞米松显著提高白细胞介素-4（Il-4）、白细胞介素-5（Il-5）和白细胞介素-13水平，而司库奇尤单抗显著抑制Il-5水平。司库奇尤单抗和地塞米松均显著降低白细胞介素-17水平。肺组织匀浆中细胞因子水平的变化部分与支气管肺泡灌洗液细胞因子相似。结论：除地塞米松外，司库奇尤单抗具有调节炎性细胞因子释放和降低小鼠急性肺损伤（叠加在加重的哮喘上）中Th17反应的能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/cd076574307b/pharmaceuticals-17-00338-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/84d98903fa8b/pharmaceuticals-17-00338-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/8f3b53981c07/pharmaceuticals-17-00338-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/f713ed512a24/pharmaceuticals-17-00338-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/7d557e6090fc/pharmaceuticals-17-00338-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/bc9497590442/pharmaceuticals-17-00338-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/144676994545/pharmaceuticals-17-00338-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/cd076574307b/pharmaceuticals-17-00338-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/84d98903fa8b/pharmaceuticals-17-00338-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/8f3b53981c07/pharmaceuticals-17-00338-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/f713ed512a24/pharmaceuticals-17-00338-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/7d557e6090fc/pharmaceuticals-17-00338-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/bc9497590442/pharmaceuticals-17-00338-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/144676994545/pharmaceuticals-17-00338-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c98/10974991/cd076574307b/pharmaceuticals-17-00338-g007.jpg

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