Cholinergic stimulation attenuates the IL-4 induced expression of E-selectin and vascular endothelial growth factor by equine pulmonary artery endothelial cells.
Abstract: The endothelium plays a critical role in regulating leukocyte recruitment and migration during inflammation. Recent studies provide evidence that acetylcholine (ACh) and other cholinergic mediators block endothelial cells activation and leukocyte recruitment during inflammation. We thus postulated that the non-neuronal cholinergic system might modulate the recruitment of neutrophils during allergic pulmonary inflammation. In the present study, we examined the effects of cholinergic stimulation on the expression of neutrophil chemokines and adhesion molecules by endothelial cells stimulated by recombinant equine (re) IL-4. Using primary equine pulmonary artery endothelial cells culture and real-time RT-PCR method, we observed that ACh, nicotine, and muscarine inhibit the expression of E-selectin and vascular endothelial growth factor by endothelial cells stimulated by reIL-4. The expression of CXCL-8, a potent neutrophil chemotactic cytokine, remained unaffected however. These findings suggest that the cholinergic anti-inflammatory pathway may modulate pulmonary allergic inflammation and remodeling by the inhibition of selected adhesion molecules and growth factors.
Publication Date: 2009-05-18 PubMed ID: 19501920DOI: 10.1016/j.vetimm.2009.05.003Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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This study is about how cholinergic stimulation limits the expression of certain molecules associated with inflammation in the lungs, possibly reducing allergic inflammation in this area.
Research Background
- The endothelium (inner layer of blood vessels) plays a crucial role in controlling the movement of white blood cells during inflammation, an important aspect of the body’s immune response.
- Earlier studies have shown that acetylcholine (ACh) and other cholinergic mediators reduce the activation of endothelial cells and the recruitment of white blood cells during inflammation.
- The researchers formulated a hypothesis that the non-neuronal cholinergic system (the part of the nervous system that doesn’t involve neurons) might alter the recruitment of neutrophils, a type of white blood cell, during allergic inflammation in the lungs.
Research Methodology and Findings
- In this study, the effects of cholinergic stimulation on the expression of neutrophil chemokines and adhesion molecules by endothelial cells were examined. These cells were stimulated using recombinant equine (re) IL-4, which is an immune protein produced by certain white blood cells.
- The researchers used a culture of primary equine pulmonary artery endothelial cells and a method called real-time RT-PCR.
- They found that ACh, nicotine, and muscarine (which are all molecules that can stimulate the cholinergic system) inhibit the expression of E-selectin and vascular endothelial growth factor. Both E-selectin and vascular endothelial growth factor play roles in inflammation, with E-selectin helping white blood cells stick to the endothelium, and vascular endothelial growth factor promoting the formation of new blood vessels.
- Despite these effects, the expression of CXCL-8, a molecule that attracts neutrophils, was not affected.
Conclusion
- The findings suggest that the cholinergic anti-inflammatory pathway (the part of the immune system that uses acetylcholine and other similar molecules to control inflammation) might influence allergic inflammation in the lungs.
- It could do this by inhibiting key molecules involved in inflammation and the formation of new blood vessels.
Cite This Article
APA
Huang H, Lavoie-Lamoureux A, Lavoie JP.
(2009).
Cholinergic stimulation attenuates the IL-4 induced expression of E-selectin and vascular endothelial growth factor by equine pulmonary artery endothelial cells.
Vet Immunol Immunopathol, 132(2-4), 116-121.
https://doi.org/10.1016/j.vetimm.2009.05.003 Publication
Researcher Affiliations
- Department of Clinical Sciences, Faculty of Veterinary Medicine, Université de Montréal, C.P. 5000, 3200 Sicotte, Saint-Hyacinthe, Québec, Canada, J2S 7C6. huanghong@tjh.tjmu.edu.cn
MeSH Terms
- Acetylcholine / pharmacology
- Animals
- Base Sequence
- Cells, Cultured
- Cholinergic Agents / pharmacology
- DNA Primers / genetics
- E-Selectin / genetics
- Endothelial Cells / drug effects
- Endothelial Cells / immunology
- Endothelial Cells / physiology
- Gene Expression / drug effects
- Horses / genetics
- Horses / immunology
- Horses / physiology
- Interleukin-4 / pharmacology
- Interleukin-8 / genetics
- Muscarine / pharmacology
- Nicotine / pharmacology
- Pulmonary Artery / drug effects
- Pulmonary Artery / immunology
- Pulmonary Artery / physiology
- RNA, Messenger / genetics
- RNA, Messenger / metabolism
- Recombinant Proteins / pharmacology
- Vascular Endothelial Growth Factor A / genetics
Citations
This article has been cited 5 times.- Yun Y, Wang X, Xu J, Chen J, Wang X, Yang P, Qin L. Optogenetic stimulation of basal forebrain cholinergic neurons prevents neuroinflammation and neuropsychiatric manifestations in pristane induced lupus mice. Behav Brain Funct 2023 Jun 15;19(1):11.
- Yamakawa K, Matsumoto N, Imamura Y, Muroya T, Yamada T, Nakagawa J, Shimazaki J, Ogura H, Kuwagata Y, Shimazu T. Electrical vagus nerve stimulation attenuates systemic inflammation and improves survival in a rat heatstroke model. PLoS One 2013;8(2):e56728.
- Lee YW, Kim PH, Lee WH, Hirani AA. Interleukin-4, Oxidative Stress, Vascular Inflammation and Atherosclerosis. Biomol Ther (Seoul) 2010 Apr;18(2):135-144.
- Lessiak U, Melchert M, Walter I, Kummer S, Nell B, Tschulenk W, Pratscher B. Isolation-protocol, characterization, and in-vitro performance of equine umbilical vein endothelial cells. Front Vet Sci 2024;11:1421946.
- Finding EJT, Faulkner A, Nash L, Wheeler-Jones CPD. Equine Endothelial Cells Show Pro-Angiogenic Behaviours in Response to Fibroblast Growth Factor 2 but Not Vascular Endothelial Growth Factor A. Int J Mol Sci 2024 May 30;25(11).
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