Marine Natural Products and Autoimmune Diseases: From Chemistry and Molecular Mechanism to Clinical Efficacy

A special issue of Marine Drugs (ISSN 1660-3397).

Deadline for manuscript submissions: closed (31 July 2020) | Viewed by 5054

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Department of Applied Ecology, Faculty of Environmental Sciences, Czech University of Life Sciences Prague, Kamýcká 129, 165 00 Prague, Czech Republic
Interests: gene; infectious diseases; herpesviruses; pharmacology and toxicology; molecular medicine; oncology and hematology; cardiovascular diseases; natural products; drug discovery; analytical and bioanalytical techniques
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Special Issue Information

Dear Colleagues,

For decades, marine-derived drugs have played a crucial role in drug discovery development. The Nobel prize was awarded for the discovery of the natural drug Artemisinin, which has brought the therapeutic efficacy of natural product-derived chemicals into the spotlight in terms of their importance and re-established their application in clinical practice for the treatment of numerous diseases. Autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, Sjogren syndrome, ankylosing spondylitis, inflammatory bowel disease and psoriasis are increasingly becoming the primary cause of global health burdens. It is known that abnormal immune responses and inflammatory effects are implicated in the pathogenesis of autoimmune diseases. Immune-related cells (traditionally, e.g., macrophages, dendritic cells, T cells and B cells, etc., and non-traditionally, e.g., glial cells, endothelial cells, epithelial cells, fibroblasts, synovial cells and liver cells, etc.), cytokines (TNF -alpha, IL-1, 2, 4, 6, 8, 10, 17, BAFF, PGE, TGF-beta, etc.) and signal transduction (G protein-coupled receptors signaling, TNF-alpha- TRADD-TRAF2 signaling, Ras-MARPK- NF-κB signaling, BAFF-BAFFRs- -NF-κB signaling, etc.) play significant roles in the inflammatory immune responses of autoimmune diseases. Despite the efficacy of current pharmacologic strategies in the treatment of autoimmune diseases through the use of non-steroidal anti-inflammatory drugs (NSAIDs), steroidal anti-inflammatory drugs (SAIDs), and disease-modifying antirheumatic drugs (DMARDs), some of these regimens have shown undesirable effects including kidney injury, bleeding in NSAID treatment and the adverse effects of ulcers. Therefore, it is crucial to search for new sources such as marine sources that provide less undesirable side effects as well as new mechanisms of action. The therapeutic effect of these drugs succeeds by regulating inflammatory responses and the abnormal immune response involved in autoimmune diseases.

The aim of this Special Issue is to shed light on the role of marine-derived drugs and strengthen their application in clinical practice for the treatment of autoimmune diseases through regulating abnormal immune responses and inflammatory effects, which are involved in autoimmune diseases. We encourage the submission of original research articles (preclinical and clinical studies) and reviews that make a novel and substantial contributions to the scientific community.

Dr. Sherif T. S. Hassan
Guest Editor

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Keywords

  • marine natural products
  • autoimmune diseases
  • abnormal immune response
  • inflammatory effects
  • immune-related cells
  • preclinical and clinical studies

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Published Papers (1 paper)

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Research

13 pages, 1312 KiB  
Article
A Microbiological, Toxicological, and Biochemical Study of the Effects of Fucoxanthin, a Marine Carotenoid, on Mycobacterium tuberculosis and the Enzymes Implicated in Its Cell Wall: A Link Between Mycobacterial Infection and Autoimmune Diseases
by Miroslava Šudomová, Mohammad Ali Shariati, Javier Echeverría, Ioana Berindan-Neagoe, Seyed Mohammad Nabavi and Sherif T. S. Hassan
Mar. Drugs 2019, 17(11), 641; https://doi.org/10.3390/md17110641 - 14 Nov 2019
Cited by 18 | Viewed by 4032
Abstract
This study explored the antitubercular properties of fucoxanthin, a marine carotenoid, against clinical isolates of Mycobacterium tuberculosis (Mtb). Two vital enzymes involved in Mtb cell wall biosynthesis, UDP-galactopyranose mutase (UGM) and arylamine-N-acetyltransferase (TBNAT), were selected as drug targets to reveal the [...] Read more.
This study explored the antitubercular properties of fucoxanthin, a marine carotenoid, against clinical isolates of Mycobacterium tuberculosis (Mtb). Two vital enzymes involved in Mtb cell wall biosynthesis, UDP-galactopyranose mutase (UGM) and arylamine-N-acetyltransferase (TBNAT), were selected as drug targets to reveal the mechanism underlying the antitubercular effect of fucoxanthin. The obtained results showed that fucoxanthin showed a clear bacteriostatic action against the all Mtb strains tested, with minimum inhibitory concentrations (MIC) ranging from 2.8 to 4.1 µM, along with a good degree of selectivity index (ranging from 6.1 to 8.9) based on cellular toxicity evaluation compared with standard drug isoniazid (INH). The potent inhibitory actions of fucoxanthin and standard uridine-5’-diphosphate against UGM were recorded to be 98.2% and 99.2%, respectively. TBNAT was potently inactivated by fucoxanthin (half maximal inhibitory concentration (IC50) = 4.8 µM; 99.1% inhibition) as compared to INH (IC50 = 5.9 µM; 97.4% inhibition). Further, molecular docking approaches were achieved to endorse and rationalize the biological findings along with envisaging structure-activity relationships. Since the clinical evidence of the last decade has confirmed the correlation between bacterial infections and autoimmune diseases, in this study we have discussed the linkage between infection with Mtb and autoimmune diseases based on previous clinical observations and animal studies. In conclusion, we propose that fucoxanthin could demonstrate great therapeutic value for the treatment of tuberculosis by acting on multiple targets through a bacteriostatic effect as well as by inhibiting UGM and TBNAT. Such outcomes may lead to avoiding or decreasing the susceptibility to autoimmune diseases associated with Mtb infection in a genetically susceptible host. Full article
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