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Special Issue "Neutrophil Extracellular Trap (NET) Formation: Mechanism, Disease and Drugs"
A special issue of Biomolecules (ISSN 2218-273X).
Deadline for manuscript submissions: 31 December 2019.
Interests: NET formation; molecular mechanisms; kinases; mitochondria; transcriptional firing; a unified model of NET formation; lipid mediators; apoptosis during NET formation (ApoNETosis); pH; iPS-derived neutrophils; inflammatory lung diseases sepsis; cystic fibrosis; rare lung diseases; innate immune proteins; complement; drugs for regulating NET formation
Interests: Granulocyte functions; molecular mechanisms of NET and EET formation; apoptosis; necroptosis and autophagy in inflammatory diseases and cancer. Pathogenic mechanisms of atopic dermatitis; hypereosinophilic syndromes; eosinophilic esophagitis; bullous pemphigoid and malignant melanoma; identification of new drug targets; in vitro and in vivo test systems to determine the effects of drugs on the immune system; and participation in clinical drug studies
Interests: Neutrophil and macrophage function in bacterial infection; NETs; innate immune signaling; molecular pathogenesis of streptococcal and staphylococcal infections; glycobiology of host-pathogen interactions; novel approaches to treat antibiotic-resistance and sepsis including virulence factor inhibition; immune boosting and drug repurposing
Extensive research work conducted over the last decade shows that neutrophils and certain other immune cells release chromatin and mitochondrial DNA coated with antimicrobial peptides and proteases as extracellular traps (NETs). NET formation is a complex process involving multiple steps, including NADPH oxidase-mediated and mitochondrial ROS production, glycolytic ATP production, activation of the cytoskeleton, kinase cascades, granular proteins coating DNA, and increases in intracellular calcium. Several studies suggest that different types of cell death could lead to NET formation (NETosis, autophagic cell death, necroptosis).
Different agonists, cell–cell interactions, external millilux, and intercellular changes regulate NET formations in various infectious, inflammatory, and autoimmune diseases. The involvement of NETs in several other diseases including cancer and cardiovascular conditions has also been reported. Relative contributions of NETs to microbial killing, compared to other tissue-specific microbicidal innate immune proteins and pathways such as complement activation, are also not fully explored. Although NETs have been considered an important antimicrobial component, it is now apparent that NETs are detrimental when formed out of context, especially during chronic inflammatory conditions.
Once NETs are released, they may be degraded by nucleases and cleared by phagocytes including macrophages. Breaking NETs with DNase I is reported to reduce tissue damage. However, suppressing excess NET formation is now considered a useful option to limit the negative effects of NETs while maintaining the phagocytic functions of neutrophils. Drugs that would regulate NET formation may hold therapeutic potential for treating NET-related diseases.
For this Special Issue, we encourage the submission of articles that describe novel mechanistic insights, NET formation agonists and antagonists, and potential drugs, for various NET-related diseases and conditions.
Dr. Nades Palaniyar
Dr. Hans-Uwe Simon
Dr. Victor Nizet
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- Neutrophil extracellular traps (NETs); NETosis; ApoNETosis; necroptosis; pyroptosis; cytoplast formation
- ET formation by other immune cells; platelets
- molecular mechanisms; NADPH oxidase-dependent NET formation; NADPH oxidase-independent NET formation
- Reactive oxygen and nitrogen species; kinases; histone modification; transcription; calcium-dependent Net formation; mitochondria; granular proteins; cytoskeleton; nuclear membrane
- NET formation agonists and antagonists
- Complement; innate immune proteins
- NET-mediated killing
- drugs that regulate NET formation
- NET clearance
- NET-mediated diseases including infection; inflammation; autoimmune diseases; nephritis; cancer; cardiovascular diseases and others