Emodin alleviates LPS-induced inflammatory response in lung injury rat by affecting the function of granulocytes

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Abstract

Background

Acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) are critical life-threatening syndromes characterized by the infiltration of a large number of granulocytes (mainly neutrophils) that lead to an excessive inflammatory response. Emodin (Emo) is a naturally occurring anthraquinone derivative and an active ingredient of Chinese medicine. It is believed to have anti-inflammatory effects. In this study, we examined the impact of Emo on the pulmonary inflammatory response and the granulocytes function in a rat model of lipopolysaccharide (LPS)-induced ALI.

Results

Treatment with Emo protected rat against LPS-induced ALI. Compared to untreated rat, Emo-treated rat exhibited significantly ameliorated lung pathological changes and decreased tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). However, Emo has no protective effect on the rat model of acute lung injury with granulocyte deficiency. In addition, treatment with Emo enhanced the bactericidal capacity of LPS-induced granulocytes via the up-regulation of the ability of granulocytes to phagocytize bacteria and generate neutrophil extracellular traps (NETs). Emo also downregulated the respiratory burst and the expression of reactive oxygen species (ROS) in LPS-stimulated granulocytes, alleviating the damage of granulocytes to surrounding tissues. Finally, Emo can accelerate the resolution of inflammation by promoting apoptosis of granulocytes.

Conclusion

Our results provide the evidence that Emo could ameliorates LPS-induced ALI via its anti-inflammatory action by modulating the function of granulocytes. Emo may be a promising preventive and therapeutic agent in the treatment of ALI.

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Most cited references 21

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Points of control in inflammation.

Carl Nathan (2002)

Inflammation is a complex set of interactions among soluble factors and cells that can arise in any tissue in response to traumatic, infectious, post-ischaemic, toxic or autoimmune injury. The process normally leads to recovery from infection and to healing, However, if targeted destruction and assisted repair are not properly phased, inflammation can lead to persistent tissue damage by leukocytes, lymphocytes or collagen. Inflammation may be considered in terms of its checkpoints, where binary or higher-order signals drive each commitment to escalate, go signals trigger stop signals, and molecules responsible for mediating the inflammatory response also suppress it, depending on timing and context. The non-inflammatory state does not arise passively from an absence of inflammatory stimuli; rather, maintenance of health requires the positive actions of specific gene products to suppress reactions to potentially inflammatory stimuli that do not warrant a full response.

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Priming of the neutrophil respiratory burst: role in host defense and inflammation.

Jamel El-Benna, Margarita Hurtado-Nedelec, Viviana Marzaioli … (2016)

Neutrophils are the major circulating white blood cells in humans. They play an essential role in host defense against pathogens. In healthy individuals, circulating neutrophils are in a dormant state with very low efficiency of capture and arrest on the quiescent endothelium. Upon infection and subsequent release of pro-inflammatory mediators, the vascular endothelium signals to circulating neutrophils to roll, adhere, and cross the endothelial barrier. Neutrophils migrate toward the infection site along a gradient of chemo-attractants, then recognize and engulf the pathogen. To kill this pathogen entrapped inside the vacuole, neutrophils produce and release high quantities of antibacterial peptides, proteases, and reactive oxygen species (ROS). The robust ROS production is also called 'the respiratory burst', and the NADPH oxidase or NOX2 is the enzyme responsible for the production of superoxide anion, leading to other ROS. In vitro, several soluble and particulate agonists induce neutrophil ROS production. This process can be enhanced by prior neutrophil treatment with 'priming' agents, which alone do not induce a respiratory burst. In this review, we will describe the priming process and discuss the beneficial role of controlled neutrophil priming in host defense and the detrimental effect of excessive neutrophil priming in inflammatory diseases.

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Author and article information

Contributors

Feng Qi:

ORCID: http://orcid.org/0000-0001-9550-0814

qifeng66821@sina.com

Journal

Journal ID (nlm-ta): J Inflamm (Lond)

Journal ID (iso-abbrev): J Inflamm (Lond)

Title: Journal of Inflammation (London, England)

Publisher: BioMed Central (London )

ISSN (Electronic): 1476-9255

Publication date (Electronic): 8 August 2020

Publication date PMC-release: 8 August 2020

Publication date Collection: 2020

Volume: 17

Electronic Location Identifier: 26

Affiliations

[1 ]Department of Anesthesiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012 Shandong Province China

[2 ]GRID grid.417384.d, ISNI 0000 0004 1764 2632, Department of Anesthesiology, , The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, ; Wenzhou, 325000 Zhejiang Province China

Author information

Feng Qi http://orcid.org/0000-0001-9550-0814

Article

Publisher ID: 252

DOI: 10.1186/s12950-020-00252-6

PMC ID: 7414666

PubMed ID: 32782444

SO-VID: 53904760-6d3b-4034-99a0-8aaccb81ba90

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 23 January 2020

Date accepted : 30 July 2020

Funding

Funded by: the National Natural Science Foundation of China

Award ID: 81672250

Award Recipient : Feng Qi

Funded by: Zhejiang Natural Science Foundation

Award ID: LQ15H010002

Award Recipient : Hongxia Mei

Funded by: Project of Wenzhou Science and Technology Bureau

Award ID: Y20140084

Award Recipient : Hongxia Mei

Custom metadata

ScienceOpen disciplines: Immunology

Keywords: emodin,granulocytes,acute lung injury (ali),acute respiratory distress syndrome (ards)

Data availability:

ScienceOpen disciplines: Immunology

Keywords: emodin, granulocytes, acute lung injury (ali), acute respiratory distress syndrome (ards)

Emodin alleviates LPS-induced inflammatory response in lung injury rat by affecting the function of granulocytes

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Abstract

Background

Results

Conclusion

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Gamma Delta T cells

Most cited references 21

Points of control in inflammation.

How leukocytes cross the vascular endothelium.

Priming of the neutrophil respiratory burst: role in host defense and inflammation.

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Contributors

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