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Antibiotics
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New Insights Toward the Development of Novel Inhibitors of S....
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New Insights Toward the Development of Novel Inhibitors of S. aureus and P. aeruginosa Factors

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

Deadline for manuscript submissions: 15 June 2026 | Viewed by 5752

Special Issue Editors

Dr. Que Chi Truong-Bolduc

E-Mail Website
Guest Editor
Division of Infectious Diseases and Medical Services, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
Interests: anti-bacterial agents; efflux pumps and transporters; genes regulator; microbial interaction; microbial regulation; multidrug resistance-associated proteins; Staphylococcus aureus; Pseudomonas aeruginosa
Dr. Leon G. Leanse

E-Mail Website
Guest Editor
Europa Point Campus, University of Gibraltar, Gibraltar, Gibraltar
Interests: antimicrobial resistance (AMR); public health; non-traditional antimicrobial approaches; superbug
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Hidemasa Nakaminami

E-Mail Website
Guest Editor
Department of Clinical Microbiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, Japan
Interests: MRSA; molecular epidemiology; antibiotic resistance; pathogenicity
Dr. Chun-Hsing Liao

E-Mail Website
Guest Editor
Department of Internal Medicine, Far Eastern Memorial Hospital, New Taipei City, Taiwan
Interests: S. aureus; K. pneumoniae; infection control

Special Issue Information

Dear Colleagues,

Staphylococcus aureus and Pseudomonas aeruginosa, both classified among the ESKAPE pathogens, represent a growing public health concern due to their increasing multidrug resistance and the limited development of new antimicrobial therapies. P. aeruginosa possesses three interconnected quorum-sensing (QS) circuits regulated by MvfR, LasR, and RhlR, which are central to P. aeruginosa’ s virulence and antibiotic resistance mechanisms. MvfR (formerly known as PqsR) is a major regulator of multiple P. aeruginosa virulence factors and plays a crucial role in acute, persistent, and relapsing infections. MvfR influences the expressions of LasR and RhlR, and both contribute to P. aeruginosa’ s competition with other microbes via the production of siderophores (pyoverdine, pyochelin) and phenazines (pyocyanin). RhlR directly regulates P. aeruginosa virulent factor rhamnolipids. S. aureus infections pose a significant challenge due to the involved virulence factors and increasing antibiotic resistance. S. aureus utilizes surface proteins to bind host cells and tissues or employs protein A to bind to antibodies and block the host’s immune response. S. aureus secretes various toxins that cause tissue destruction and systemic toxicity, and it forms biofilms that act as a protective barrier against antibiotics and the host immune system. A coinfection with S. aureus and P. aeruginosa increases severity and complications in patients with cystic fibrosis, wound infections, and respiratory infections. The coexistence of S. aureus and P. aeruginosa can increase antibiotic resistance due to a mix of biofilms, an enhanced tolerance to certain antibiotics, and an altered pattern of gene expression leading to an increase in the expression of genes associated with antibiotic resistance. This Special Issue seeks manuscript submissions that further our understanding of antimicrobial resistance in the coinfection of S. aureus and P. aeruginosa, as well as new approaches toward the development of novel strategies to inhibit S. aureus and P. aeruginosa components. Contributions on combination therapy, anti-biofilm strategies, or targeting microbial interactions and host response are especially encouraged.

Dr. Que Chi Truong-Bolduc
Dr. Leon G. Leanse
Prof. Dr. Hidemasa Nakaminami
Dr. Chun-Hsing Liao
Guest Editors

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 250 words) can be sent to the Editorial Office for assessment.

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

  • MSSA
  • MRSA
  • P. aeruginosa
  • coinfection
  • antibiotic resistance
  • therapeutic strategy
  • anti-virulence
  • quorum-sensing
  • virulence factors
  • biofilms

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Published Papers (4 papers)

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Research

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15 pages, 1075 KB  
Article
Synergistic Antibacterial Activity of Azithromycin-Loaded Chitosan Nanoparticles Alone and in Combination with Cetirizine Dihydrochloride Against Resistant Isolates of Respiratory Tract Infections
by Umbreen Anwar, Adeel Sattar, Muhammad Adil Rasheed, Muhammad Abu Bakr Shabbir and Mateen Abbas
Antibiotics 2025, 14(10), 992; https://doi.org/10.3390/antibiotics14100992 - 3 Oct 2025
Viewed by 1885
Abstract
Background/Objectives: Antibiotic resistance is a major public health concern, with considerable socio-economic consequences. Researchers are exploring alternative strategies, including nanotechnology, which has shown significance in targeted drug delivery. This study evaluates the synergistic antibacterial activity of azithromycin-loaded chitosan nanoparticles (AZM-CSNPs) against azithromycin-resistant clinical [...] Read more.
Background/Objectives: Antibiotic resistance is a major public health concern, with considerable socio-economic consequences. Researchers are exploring alternative strategies, including nanotechnology, which has shown significance in targeted drug delivery. This study evaluates the synergistic antibacterial activity of azithromycin-loaded chitosan nanoparticles (AZM-CSNPs) against azithromycin-resistant clinical respiratory isolates of methicillin-resistant Staphylococcus aureus (MRSA) and Klebsiella pneumoniae (K. pneumoniae). Methods: A total of 87 sputum samples (n = 87) were collected and analyzed. The ermB gene for K. pneumoniae and the ermA gene for MRSA were used to confirm resistant isolates. Among 87 samples, 29 manifested K. pneumoniae, and 32 exhibited MRSA-positive cultures, confirmed through phenotypic and genotypic methods. The RT-PCR is performed by using a cDNA Kit to determine the gene expression. Results: The results elucidate resistance of K. pneumoniae against several antibiotics, including azithromycin (15 µg), chloramphenicol (30 µg), and amoxicillin (30 µg), while MRSA also showed resistance to cefoxitin (30 µg), azithromycin (15 µg), and gentamycin (10 µg). Reduction in the MIC value of the nanoparticle formulation showed their effectiveness. The AZM-CSNPs combined with cetirizine dihydrochloride helped to down-regulate the resistant genes. Conclusions: Notably, a strong synergistic effect was observed with AZM-CSNPs in combination with cetirizine, significantly enhancing antibacterial efficacy against resistant isolates. Full article
(This article belongs to the Special Issue New Insights Toward the Development of Novel Inhibitors of S. aureus and P. aeruginosa Factors)
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25 pages, 3491 KB  
Article
Selective Targeting and Enhanced Photodynamic Inactivation of Methicillin-Resistant Staphylococcus aureus (MRSA) by a Decacationic Vancomycin–Mesochlorin Conjugate
by He Yin, Xiaojing Liu, Min Wang, Ying Wang, Tianhong Dai and Long Y. Chiang
Antibiotics 2025, 14(10), 978; https://doi.org/10.3390/antibiotics14100978 - 28 Sep 2025
Viewed by 1153
Abstract
Background/Objectives: Covalent conjugation of an antibiotic vancomycin (VCM) moiety and a photosensitizing mesochlorin (mChlPd) unit into one molecular entity may present the potential to produce the combinatorial effect of both antibacterial photodynamic therapeutic (aPDT) and antibiotic activities. Our recent [...] Read more.
Background/Objectives: Covalent conjugation of an antibiotic vancomycin (VCM) moiety and a photosensitizing mesochlorin (mChlPd) unit into one molecular entity may present the potential to produce the combinatorial effect of both antibacterial photodynamic therapeutic (aPDT) and antibiotic activities. Our recent study indicated that a short linkage of <4 (C−C/or C−N) bond distances between these two moieties resulted in significant steric hindrance due to the bulky VCM, which greatly reduces the accessibility of the agent to the cell surface of methicillin-resistant Staphylococcus aureus (MRSA). The observed aPDT efficacy was found to be minimal. Here, we report that the revision of this linkage, via an EG10 unit using identical synthetic procedures, was able to resolve the issue. Methods: Accordingly, the corresponding combinatorial aPDT−antibiotic compound, consisting of two covalently bonded quaternary ammonium pentacationic arms on the mesochlorin chromophore core, designated as VCMe-mChlPd-N10+ (LC40e+), was prepared for applications in antibacterial photodynamic inactivation (aPDI) activity. It was selected to investigate its enhanced binding and targeting ability to the surface of Gram-positive MRSA cells. Subsequent antibacterial photodynamic therapeutic (aPDT) activity to inactivate MRSA was investigated to substantiate the corresponding cell-surface binding effect on the efficacy of aPDT. Results: We found that the covalent combination of 10 positive charges and an MRSA-targeting vancomycin (VCM) moiety in a conjugated structure, functioning as an antibiotic–decacationic photosensitizing agent (Abx-dcPS), was capable of largely improving the MRSA cell-targeting efficiency. Importantly, variation in the chain length of the oligo(ethylene glycol) linker of VCMe-mChlPd-N10+, which was sufficiently long enough to properly separate the photoactive mesochlorin ring moiety from the VCM moiety within the molecular structure, resulted in significantly enhanced aPDT activity. The new conjugate provided nearly complete eradication (>6.5-log10 colony-forming units (CFU) reduction) of MRSA cells in vitro. The aPDT efficacy followed the order Abx-dcPS (combinatorial decacationic) > dcPS (decacationic) >> nPS (nonionic). This order was also verified by the relative physical binding trend of these PSs using either nPS-, dcPS-, or Abx-dcPS-pretreated and pre-fixed MRSA cells in investigations of fluorescent confocal microscopy, UV–vis fluorescence spectroscopy, and transmission electron microscopy (TEM). Conclusions: Furthermore, the molecular conjugate of Abx-dcPS may provide covalent co-delivery of two drug components concurrently, which might also serve as an effective antibiotic agent after aPDT and potentially prevent the reoccurrence of MRSA-induced infection. Full article
(This article belongs to the Special Issue New Insights Toward the Development of Novel Inhibitors of S. aureus and P. aeruginosa Factors)
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Review

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22 pages, 2039 KB  
Review
Phage-Based Approaches to Chronic Pseudomonas aeruginosa Lung Infection in Cystic Fibrosis
by Wontae Hwang, Ji Hyun Yong, Bryan R. Lenneman and Lael M. Yonker
Antibiotics 2026, 15(2), 125; https://doi.org/10.3390/antibiotics15020125 - 27 Jan 2026
Viewed by 1715
Abstract
Chronic Pseudomonas aeruginosa lung infections in cystic fibrosis (CF) represent one of the most treatment-refractory bacterial diseases, sustained by biofilm formation, metabolic dormancy, and adaptive antibiotic resistance evolution. While bacteriophage (phage) therapy has emerged as a promising alternative for multidrug-resistant (MDR) pathogens, clinical [...] Read more.
Chronic Pseudomonas aeruginosa lung infections in cystic fibrosis (CF) represent one of the most treatment-refractory bacterial diseases, sustained by biofilm formation, metabolic dormancy, and adaptive antibiotic resistance evolution. While bacteriophage (phage) therapy has emerged as a promising alternative for multidrug-resistant (MDR) pathogens, clinical studies in CF have demonstrated transient reductions in bacterial burden without achieving complete eradication. This review integrates molecular, evolutionary, and immunological findings to explain the multifactorial barriers that limit phage therapeutic efficacy in chronic CF infections. We highlight three major obstacles: (i) bacterial dormancy and persistence within biofilms that restrict phage adsorption and replication; (ii) hypermutability and extensive genotypic diversification of CF-adapted P. aeruginosa, which accelerate phage resistance evolution and necessitate broad host-range coverage; and (iii) CF-specific immune constraints—including a dysfunctional innate immune system and phage-neutralizing humoral immunity—that reduce phage bioavailability and undermine sustained bacterial clearance. Emerging strategies to overcome these challenges include the discovery of dormant-targeting phages capable of replicating in metabolically quiescent cells, evolution-informed phage training to delay resistance evolution, and synthetic phage engineering approaches designed to disrupt biofilms and expand host-range coverage. In parallel, computational or artificial intelligence (AI)-guided frameworks for phage cocktail design and cystic fibrosis transmembrane conductance regulator (CFTR) modulator-mediated restoration of host immune function together offer a more integrated therapeutic paradigm that unites phage biology and host immune context. By unifying clinical outcomes with mechanistic, evolutionary, and immunological perspectives, this review outlines a next-generation framework for phage therapy in CF aimed at achieving more durable therapeutic outcomes. Full article
(This article belongs to the Special Issue New Insights Toward the Development of Novel Inhibitors of S. aureus and P. aeruginosa Factors)
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Other

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10 pages, 221 KB  
Perspective
Epidemiologic and Clinical Divergence of MRSA USA100 and USA300 in the United States
by Camille André and Michael S. Gilmore
Antibiotics 2026, 15(4), 372; https://doi.org/10.3390/antibiotics15040372 - 4 Apr 2026
Viewed by 572
Abstract
Methicillin-resistant S. aureus (MRSA) is listed by the World Health Organization as a priority pathogen posing a major worldwide threat to public health. Two lineages of MRSA predominate as causes of human infections in the U.S.: USA300 and USA100. Although they are most [...] Read more.
Methicillin-resistant S. aureus (MRSA) is listed by the World Health Organization as a priority pathogen posing a major worldwide threat to public health. Two lineages of MRSA predominate as causes of human infections in the U.S.: USA300 and USA100. Although they are most often grouped together as MRSA, these two lineages differ in pathogenetic mechanisms in important ways. The epidemic spread of these two dominant lineages has been problematic because of the multidrug-resistant profile of USA100 and the virulence of USA300, as well as their ability to adapt to both community and hospital environments. In this perspective, we examine what is currently known about their distinctive biology and the consequent differences in infections caused by these two main MRSA epidemic clones. The purpose of this perspective is to provide critical insights to the clinical microbiology community to stimulate further research to inform the design of new prevention and management strategies for MRSA. Full article
(This article belongs to the Special Issue New Insights Toward the Development of Novel Inhibitors of S. aureus and P. aeruginosa Factors)
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