Published in: First Personal Medical Congress
COI code: IPMCMED01_005
Paper Language: English
How to Download This Paper
For Downloading the Fulltext of CIVILICA papers please visit the orginal Persian Section of website.
Authors Modulation of neutrophil extracellular trap formation in health and diseaseAva Hosseinzadeh - Division of Immunology, Department of Clinical Microbiology, Umeå University, Sweden
Constantin Urban - Division of Immunology, Department of Clinical Microbiology, Umeå University, Sweden
Abstract:The critical prompt innate immune response is highly built upon the influx of neutrophils from the blood stream to the site of infection. In the battlefield, neutrophils sense pathogen-associated molecular patterns (PAMPs) through their pattern-recognition receptors (PRRs) to launch a number of responses with the goal to defeat the invading pathogen. Neutrophils wide spectrum of responses ranges from reactive oxygen species production (ROS), phagocytosis, cytokine secretion, and neutrophil extracellular trap (NET) formation. The NET scaffold is composed of nuclear chromatin which is armed with antimicrobial proteins. DNA traps are able to ensnare and kill microbes. NETs impose deleterious effects on the host itself in addition to their antimicrobial activity. These hazardous effects mainly stem from pro-inflammatory and tissue-destructive activity of NETs. Therefore, it seems rational that NET formation is tightly regulated and not happening spontaneously. Positive and negative regulators of NET formation were investigated in a mechanistic fashion. As unbalanced inflammation is harmful to the host, we aimed to find molecules, which are able to inhibit NET formation. Thus, we introduced the non-toxic agent tempol that efficiently blocked NET induction. We therefore proposed tempol as a potential treatment during inflammatory disorders where NET formation is out of balance. In quest for positive regulators of NET formation we found the major addictive component of tobacco and electronic cigarettes, nicotine, as compelling direct inducer of NET release. Interestingly, nicotine is associated with exacerbated inflammatory diseases exerting its pro-inflammatory activity via acetylcholine receptor by targeting protein kinase B activation with no effect on NADPH oxidase complex in a ROS independent fashion. In consideration of neutrophils role in smoking-related diseases we propose targeting Akt could lower the undesirable effect of NET. In conclusion, we identified new modulators of NET formation which might have implications in forthcoming therapies.
Keywords:neutrophil extracellular trap (NET), Candida albicans, Tempol, Nicotine
COI code: IPMCMED01_005
how to cite to this paper:If you want to refer to this article in your research, you can easily use the following in the resources and references section:
Hosseinzadeh, Ava & Constantin Urban, 2016, Modulation of neutrophil extracellular trap formation in health and disease, First Personal Medical Congress, تهران, دانشگاه علوم پزشكي ايران - پژوهشكده ملي مهندسي ژنتيك و زيست فناوري ايران، مركز همكاري هاي فناوري و نوآوري هاي رياست جمهوري, https://www.civilica.com/Paper-IPMCMED01-IPMCMED01_005.htmlInside the text, wherever referred to or an achievement of this article is mentioned, after mentioning the article, inside the parental, the following specifications are written.
First Time: (Hosseinzadeh, Ava & Constantin Urban, 2016)
Second and more: (Hosseinzadeh & Urban, 2016)
For a complete overview of how to citation please review the following CIVILICA Guide (Citation)