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Antibiotics
Special Issues
Antimicrobial Drug Discovery: New Theories and New Therapies
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Antimicrobial Drug Discovery: New Theories and New Therapies

A special issue of Antibiotics (ISSN 2079-6382). This special issue belongs to the section "Novel Antimicrobial Agents".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 4707

Special Issue Editor

Prof. Dr. Ki-Young Kim

E-Mail Website
Guest Editor
Graduate School of Biotechnology, Kyung Hee University, Seocheon, Giheung, Yongin, Gyeonggi-do 1732, Republic of Korea
Interests: antimicrobial agents; anticancer agents; cell growth control; signal transduction; transcription regulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleague,

An antimicrobial drug is a compound that is used to treat and control microbial pathogens toward preventing infections in humans, animals and plants. Antimicrobial resistance threatens the effective prevention and treatment of infections caused by bacteria, parasites, viruses and fungi and represents one of the biggest problems currently faced by society. Strains characterized by antimicrobial resistance are arising because of the excessive use of commercially available antibiotics. More importantly, the newly discovered fungi Candida auris shows native resistance against azole antifungal agents. These concerning developments are serving as motivation toward discovering new antimicrobial drugs based on new theories and for the development and application of new therapies, which serves as the theme of this Special Issue. We welcome the submission of manuscripts addressing this theme.

Prof. Ki-Young Kim
Guest Editor

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 submissions that pass pre-check are 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. Antibiotics 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 2900 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.

Keywords

  • Antimicrobial resistance
  • Novel antibiotic drugs
  • Mechanism of drug action
  • Anti-Biofilms or biofilm formation inhibitors
  • Virulence factors
  • Host-microbial interaction
  • Synergy between new antimicrobial products and conventional antibiotics

Published Papers (2 papers)

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Research

12 pages, 1592 KiB  
Article
Pectolinarin Inhibits the Bacterial Biofilm Formation and Thereby Reduces Bacterial Pathogenicity
by Daseul Kim and Ki-Young Kim
Antibiotics 2022, 11(5), 598; https://doi.org/10.3390/antibiotics11050598 - 29 Apr 2022
Cited by 4 | Viewed by 2015
Abstract
Bacterial biofilms are a growing problem as it is a major cause of nosocomial infection from urinary catheters to chronic tissue infections and provide resistance to a variety of antibiotics and the host’s immune system. The effect of pectolinarin on the biofilm formation [...] Read more.
Bacterial biofilms are a growing problem as it is a major cause of nosocomial infection from urinary catheters to chronic tissue infections and provide resistance to a variety of antibiotics and the host’s immune system. The effect of pectolinarin on the biofilm formation in Enterococcus faecalis, Enterococcus faecium, Escherichia coli, Streptococcus mutans, Streptococcus sobrinus, Staphylococcus aureus, Pseudomonas aeruginosa, Cutibacterium acnes, and Porphyromonas gingivalis was studied in TSBg (tryptic soy broth supplemented with 1% glucose). Pectolinarin inhibited biofilm formation of E. faecalis (IC50 = 0.39 μg/mL), E. faecium (IC50 = 0.19 μg/mL), E. coli (IC50 = 0.25 μg/mL), S. mutans (IC50 = 1.2 μg/mL), S. sobrinus (IC50 = 1.4 μg/mL), S. aureus (IC50 = 0.39 μg/mL), P. aeruginosa (IC50 = 0.9 μg/mL), P. acnes (IC50 = 12.5 μg/mL), and P. gingivalis (IC50 = 9.0 μg/mL) without inhibiting the bacterial growth. Pectolinarin also showed increased susceptibility of antibacterial activity with commercially available antibiotics including ampicillin, vancomycin, streptomycin, and oxytetracyclin against E. faecalis and E. faecium. Finally, pectolinarin dose-dependently reduced the expression of genes including cytolysin genes (cylLS, cylR2 and cylM), quorum sensing (QS) genes (fsrB, fsrC, gelE, ebpA, ebpB, acm, scm and bps), and biofilm virulence genes (esp) of E. faecalis and E. faecium. Pectolinarin reduced the bacterial biofilm formation, activated the antibacterial susceptibility, and reduced the bacterial adherence. These results suggest that bacterial biofilm formation is a good target to develop the antibacterial agents against biofilm-related infections. Full article
(This article belongs to the Special Issue Antimicrobial Drug Discovery: New Theories and New Therapies)
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20 pages, 6020 KiB  
Article
Terazosin Interferes with Quorum Sensing and Type Three Secretion System and Diminishes the Bacterial Espionage to Mitigate the Salmonella Typhimurium Pathogenesis
by Wael A. H. Hegazy, Ibrahim M. Salem, Hadil Faris Alotaibi, El-Sayed Khafagy and Doaa Ibrahim
Antibiotics 2022, 11(4), 465; https://doi.org/10.3390/antibiotics11040465 - 30 Mar 2022
Cited by 29 | Viewed by 2215
Abstract
Salmonella enterica is an invasive intracellular pathogen and hires diverse systems to manipulate its survival in the host cells. Salmonella could eavesdrop on the host cells, sensing and responding to the produced adrenergic hormones and other neurotransmitters, which results in the augmentation of [...] Read more.
Salmonella enterica is an invasive intracellular pathogen and hires diverse systems to manipulate its survival in the host cells. Salmonella could eavesdrop on the host cells, sensing and responding to the produced adrenergic hormones and other neurotransmitters, which results in the augmentation of its virulence and establishes its accommodation in host cells. The current study aims to assess the anti-virulence effect of α-adrenergic antagonist terazosin on S. Typhimurium. Our findings show that terazosin significantly reduced S. Typhimurium adhesion and biofilm formation. Furthermore, terazosin significantly decreased invasion and intracellular replication of S. Typhimurium. Interestingly, in vivo, terazosin protected the mice from S. Typhimurium pathogenesis. To understand the terazosin anti-virulence activity, its effect on quorum sensing (QS), bacterial espionage, and type three secretion system (T3SS) was studied. Strikingly, terazosin competed on the membranal sensors that sense adrenergic hormones and down-regulated their encoding genes, which indicates the ability of terazosin to diminish the bacterial eavesdropping on the host cells. Moreover, terazosin significantly reduced the Chromobacterium violaceum QS-controlled pigment production and interfered with the QS receptor Lux-homolog Salmonella SdiA, which indicates the possible terazosin-mediated anti-QS activity. Furthermore, terazosin down-regulated the expression of T3SS encoding genes. In conclusion, terazosin may mitigate S. Typhimurium virulence owing to its hindering QS and down-regulating T3SS encoding genes besides its inhibition of bacterial espionage. Full article
(This article belongs to the Special Issue Antimicrobial Drug Discovery: New Theories and New Therapies)
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