Special Issue "Bacterial Stress Responses and Antibiotic Resistance Phenotypes"

A special issue of Antibiotics (ISSN 2079-6382). This special issue belongs to the section "Mechanism and Evolution of Antibiotic Resistance".

Deadline for manuscript submissions: 30 November 2021.

Special Issue Editor

Prof. Dr. Dorothea K. Thompson
E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, Campbell University, P.O. Box 1090, Buies Creek, NC 27506-1090, USA
Interests: antibiotic resistance; AmpC beta-lactamases; heavy metal stress responses in bacteria; microbial functional genomics; Cedecea opportunistic pathogens

Special Issue Information

Dear Colleagues,

Bacteria employ exquisitely controlled stress response mechanisms to survive and adapt to a myriad of growth-compromising environmental insults, including cell envelope damage, nutrient deprivation, heavy metals, oxidative and nitrosative stress, and antimicrobial drug exposure. Growing research in this area continues to demonstrate a direct linkage between stress response systems and the development of antimicrobial resistance in bacteria. Stress response genes function as determinants of antibiotic resistance, and the induction of bacterial stress response systems plays important roles in the conversion of heterogeneous resistance phenotypes to high-level, homogeneous-resistance phenotypes. This interrelationship between stress and resistance is reinforced by evidence that the inactivation of stress response genes correlates with an increased susceptibility of bacteria to antibiotics. Additionally, random stress-induced mutations (adaptive mutagenesis) also affect antibiotic resistance in bacteria. Given that the global emergence of antibiotic resistance poses an increasing threat to the effective chemotherapeutic management of infectious diseases, the molecular components comprising adaptive cellular responses to stress are a potential valuable source of new targets for clinical intervention. This Special Issue of Antibiotics is seeking manuscript submissions that advance our understanding of the stress-related molecular determinants that contribute to the development of antibiotic resistance phenotypes in bacteria. Submissions providing insight into the mechanistic link between nutrient (stringent)/cell envelope/oxidative/nitrosative stress and antibiotic resistance in bacteria are particularly encouraged

Prof. Dr. Dorothea K. Thompson
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 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. 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 1800 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

  • Bacteria
  • Stress responses
  • Stress-enhanced antibiotic resistance
  • Stress determinants of antibiotic resistance phenotypes
  • Nutrient stress
  • Cell envelope stress
  • Oxidative stress
  • Nitrosative stress

Published Papers (1 paper)

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Research

Article
In Silico Prediction and Prioritization of Novel Selective Antimicrobial Drug Targets in Escherichia coli
Antibiotics 2021, 10(6), 632; https://0-doi-org.brum.beds.ac.uk/10.3390/antibiotics10060632 - 25 May 2021
Viewed by 559
Abstract
Novel antimicrobials interfering with pathogen-specific targets can minimize the risk of perturbations of the gut microbiota (dysbiosis) during therapy. We employed an in silico approach to identify essential proteins in Escherichia coli that are either absent or have low sequence identity in seven [...] Read more.
Novel antimicrobials interfering with pathogen-specific targets can minimize the risk of perturbations of the gut microbiota (dysbiosis) during therapy. We employed an in silico approach to identify essential proteins in Escherichia coli that are either absent or have low sequence identity in seven beneficial taxa of the gut microbiota: Faecalibacterium, Prevotella, RuminococcusBacteroides, Lactobacillus, Lachnospiraceae and Bifidobacterium. We identified 36 essential proteins that are present in hyper-virulent E. coli ST131 and have low similarity (bitscore < 50 or identity < 30% and alignment length < 25%) to proteins in mammalian hosts and beneficial taxa. Of these, 35 are also present in Klebsiella pneumoniae. None of the proteins are targets of clinically used antibiotics, and 3D structure is available for 23 of them. Four proteins (LptD, LptE, LolB and BamD) are easily accessible as drug targets due to their location in the outer membrane, especially LptD, which contains extracellular domains. Our results indicate that it may be possible to selectively interfere with essential biological processes in Enterobacteriaceae that are absent or mediated by unrelated proteins in beneficial taxa residing in the gut. The identified targets can be used to discover antimicrobial drugs effective against these opportunistic pathogens with a decreased risk of causing dysbiosis. Full article
(This article belongs to the Special Issue Bacterial Stress Responses and Antibiotic Resistance Phenotypes)
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