Bacterial Infections and Antimicrobial Resistance

A Special Issue of Microorganisms (ISSN 2076-2607) belonging to the section "Antimicrobial Agents and Resistance".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 887

Editor


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Guest Editor
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, College of Life Science and Technology, Guangxi University, Nanning 530004, China
Interests: microbial pathogenesis; bacterial second messengers; antibiotic resistance; mycobacterial physiology; transcriptional regulation; host-pathogen interaction

Special Issue Information

Dear Colleagues,

The escalating crisis of antimicrobial resistance (AMR) poses a formidable challenge to global health, particularly in the context of bacterial pathogens. Diseases caused by multidrug-resistant (MDR) bacteria, including tuberculosis, are becoming increasingly difficult and sometimes impossible to treat. The intricate mechanisms behind resistance, from classic mutations and efflux pumps to the horizontal gene transfer of resistance determinants, are enabling the rapid adaptation of pathogens such as Mycobacterium tuberculosis. This Special Issue will highlight research that deepens our understanding of these mechanisms and translates findings into novel diagnostic, therapeutic, and surveillance strategies.

This Special Issue will showcase high-impact research articles and reviews focusing on the biology, genetics, and epidemiology of antibiotic-resistant bacterial pathogens. A particular emphasis will be placed on studies involving Mycobacterium species and other major human pathogenic bacteria. This Special Issue will span the full research process, from fundamental molecular studies to applied clinical and public health interventions. Our aim is to create a valuable resource that fosters collaboration and accelerates progress in combating AMR.

We invite you to submit original research articles and reviews. Suggested themes include, but are not limited to, molecular mechanisms of drug resistance in Mycobacterium tuberculosis and non-tuberculous mycobacteria; resistance and virulence in bacterial pathogens; the genomics and evolution of multidrug-resistant clones; the role of persister cells and biofilms in chronic infections; novel antimicrobial agents and therapeutic strategies; rapid diagnostic tools; host–pathogen interactions; and epidemiology and surveillance in AMR. We look forward to receiving your contributions.

Prof. Dr. Weihui Li
Guest Editor

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Keywords

  • antimicrobial resistance
  • Mycobacterium tuberculosis
  • bacterial pathogenesis
  • multidrug-resistant bacteria
  • antibiotic resistance mechanisms
  • genomics
  • novel therapeutics
  • biofilm
  • diagnostics
  • public health

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Published Papers (1 paper)

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Research

18 pages, 3553 KB  
Article
The Cyclic Di-GMP Receptor HpoR Modulates Mycobacterial Multidrug Susceptibility by Regulating IniBAC-Mediated Envelope Permeability
by Xiao Liu, Xiaocui Ling, Kun Wang, Jiachen Zheng, Hao Li, Minhao Guo, Yanzhe Ou, Jie Lu and Weihui Li
Microorganisms 2026, 14(7), 1579; https://doi.org/10.3390/microorganisms14071579 - 20 Jul 2026
Viewed by 436
Abstract
Isoniazid (INH) targets cell wall biosynthesis and is a potent antimycobacterial agent. Elucidating the regulatory networks that govern drug susceptibility in mycobacterial models is fundamental to understanding intrinsic resistance in pathogenic species. The iniBAC operon plays a crucial role in INH tolerance and [...] Read more.
Isoniazid (INH) targets cell wall biosynthesis and is a potent antimycobacterial agent. Elucidating the regulatory networks that govern drug susceptibility in mycobacterial models is fundamental to understanding intrinsic resistance in pathogenic species. The iniBAC operon plays a crucial role in INH tolerance and envelope permeability, yet the transcriptional regulatory mechanisms controlling its expression in response to INH-induced stress remain incompletely understood. The second messenger cyclic di-GMP (c-di-GMP) regulates drug susceptibility in several bacteria, but its downstream receptors and regulatory pathways in mycobacteria have not been explored. Here, we demonstrate that c-di-GMP reduces INH susceptibility via the receptor HpoR. Mechanistically, c-di-GMP alleviates HpoR-mediated repression of the iniBAC operon in a concentration-dependent manner, which decreases envelope permeability and consequently modulates multidrug susceptibility in both M. bovis BCG and M. smegmatis. This regulatory paradigm is likely conserved in pathogenic mycobacteria. Full article
(This article belongs to the Special Issue Bacterial Infections and Antimicrobial Resistance)
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