Zinc supplementation ameliorates lung injury by reducing neutrophil recruitment and activity

被引:63
|
作者
Wessels, Inga [1 ]
Pupke, Johanna Theresa [2 ]
von Trotha, Klaus-Thilo [2 ,3 ]
Gombert, Alexander [2 ]
Himmelsbach, Anika [4 ]
Fischer, Henrike Josephine [1 ]
Jacobs, Michael J. [2 ]
Rink, Lothar [1 ]
Grommes, Jochen [2 ,5 ]
机构
[1] Rhein Westfal TH Aachen, Inst Immunol, Med Fac, Aachen, Nordrhein Westf, Germany
[2] Rhein Westfal TH Aachen, Dept Vasc Surg, Med Fac, Aachen, Nordrhein Westf, Germany
[3] Marienhosp Aachen, Dept Vasc Surg, Aachen, Nordrhein Westf, Germany
[4] Rhein Westfal TH Aachen, Med Fac, Med Clin 1, Dept Cardiol, Aachen, Nordrhein Westf, Germany
[5] Rhein Maas Klinikum GmbH, Dept Vasc Surg, Wurselen, Nordrhein Westf, Germany
关键词
POLYMICROBIAL SEPSIS; TNF-ALPHA; GM-CSF; DEFICIENCY; CELLS; CHEMOTAXIS; ACTIVATION; IL-1-BETA; MODELS; GROWTH;
D O I
10.1136/thoraxjnl-2019-213357
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Introduction Zinc is well known for its anti-inflammatory effects, including regulation of migration and activity of polymorphonuclear neutrophils (PMN). Zinc deficiency is associated with inflammatory diseases such as acute lung injury (ALI). As deregulated neutrophil recruitment and their hyper-activation are hallmarks of ALI, benefits of zinc supplementation on the development of lipopolysaccharides (LPS)-induced ALI were tested. Methods 64 C57Bl/6 mice, split into eight groups, were injected with 30 mu g zinc 24 hours before exposure to aerosolised LPS for 4 hours. Zinc homoeostasis was characterised measuring serum and lung zinc concentrations as well as metallothionein-1 expression. Recruitment of neutrophils to alveolar, interstitial and intravascular space was assessed using flow cytometry. To determine the extent of lung damage, permeability and histological changes and the influx of protein into the bronchoalveolar lavage fluid were measured. Inflammatory status and PMN activity were evaluated via tumour necrosis factor a levels and formation of neutrophil extracellular traps. The effects of zinc supplementation prior to LPS stimulation on activation of primary human granulocytes and integrity of human lung cell monolayers were assessed as well. Results Injecting zinc 24 hours prior to LPS-induced ALI indeed significantly decreased the recruitment of neutrophils to the lungs and prevented their hyperactivity and thus lung damage was decreased. Results from in vitro investigations using human cells suggest the transferability of the finding to human disease, which remains to be tested in more detail. Conclusion Zinc supplementation attenuated LPS-induced lung injury in a murine ALI model. Thus, the usage of zinc-based strategies should be considered to prevent detrimental consequences of respiratory infection and lung damage in risk groups.
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页码:253 / 261
页数:9
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