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Pathogens
Special Issues
Pathogenesis, Antibiotic Resistance, and Host Immune Responses to Bacterial Infections
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Pathogenesis, Antibiotic Resistance, and Host Immune Responses to Bacterial Infections

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Bacterial Pathogens".

Deadline for manuscript submissions: closed (10 June 2026) | Viewed by 1908

Editors

Prof. Dr. Weihui Wu

E-Mail Website
Guest Editor
State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Molecular Microbiology and Technology of the Ministry of Education, Department of Microbiology, College of Life Sciences, Nankai University, Tianjin 300071, China
Interests: bacterial pathogenesis; gene regulation; antibiotic resistance
Special Issues, Collections and Topics in MDPI journals
Dr. Gukui Chen

E-Mail Website
Guest Editor
Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Xi’an 710069, China
Interests: bacterial pathogenesis; gene regulation; stress response

Special Issue Information

Dear Colleagues,

Bacterial infections remain a major global health burden, driven by the dual challenges of pathogen virulence and antimicrobial resistance. Understanding the mechanisms of bacterial pathogenesis, antibiotic resistance mechanisms, and host immune responses is critical to developing effective therapeutic and preventive strategies. This Special Issue, “Pathogenesis, Antibiotic Resistance, and Host Immune Responses to Bacterial Infections,” aims to highlight cutting-edge research that elucidates the following:

  1. How bacterial pathogens sense, manipulate, and damage host cells and tissues;
  2. The genetic, biochemical, and ecological drivers of antibiotic resistance acquisition and transmission;
  3. The innate and adaptive immune mechanisms that recognize and respond to invading bacteria.

We welcome studies exploring molecular mechanisms of virulence, antibiotic resistance, gene regulation, evolution of drug resistance, host immune responses and signaling pathways, as well as novel diagnostic or therapeutic approaches. By integrating multidisciplinary insights, this issue seeks to advance our ability to combat bacterial pathogens in an era of increasing antimicrobial resistance.

Prof. Dr. Weihui Wu
Dr. Gukui Chen
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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens 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 2200 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

  • bacterial pathogenesis
  • antibiotic resistance
  • host immune responses
  • bacterial virulence
  • antimicrobial strategies

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Published Papers (3 papers)

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Research

13 pages, 2643 KB  
Article
PvrA-Mediated Inhibition of Choline and Ethanolamine Uptake Promotes Pseudomonas aeruginosa Colonization in the Host Environment
by Shuo Wang, Liwen Yin, Jinhao Yang, Changru Zhang, Zhi Yao and Xiaolei Pan
Pathogens 2026, 15(7), 680; https://doi.org/10.3390/pathogens15070680 (registering DOI) - 26 Jun 2026
Abstract
Pseudomonas aeruginosa can utilize abundant phosphatidylcholine (PC) and phosphatidylethanolamine (PE) within the host as energy and structural substrates. Fatty acids, choline, and ethanolamine liberated from PC and PE can each serve as the sole carbon source to support bacterial growth in vitro. Our [...] Read more.
Pseudomonas aeruginosa can utilize abundant phosphatidylcholine (PC) and phosphatidylethanolamine (PE) within the host as energy and structural substrates. Fatty acids, choline, and ethanolamine liberated from PC and PE can each serve as the sole carbon source to support bacterial growth in vitro. Our previous work demonstrated that fatty acid metabolism is critical for acute pulmonary infection caused by P. aeruginosa. The pathogen senses host-derived fatty acids via the transcriptional regulator PvrA, which activates fatty acid utilization pathways and drives the production of virulence factors required for acute infection. In this study, we demonstrate that during acute pulmonary infection in mice, P. aeruginosa upregulates fatty acid catabolism while simultaneously repressing choline and ethanolamine uptake and metabolism pathways. Deletion of the transcriptional activators GbdR and EatR (which control choline and ethanolamine utilization respectively) enhances pulmonary bacterial colonization. We further identify fatty acids as environmental signals that trigger repression of choline and ethanolamine utilization programs. PvrA mediates this signaling cascade by directly binding to the promoters of gbdR and eatR and suppressing their transcription upon fatty acid exposure. Full article
(This article belongs to the Special Issue Pathogenesis, Antibiotic Resistance, and Host Immune Responses to Bacterial Infections)
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15 pages, 1534 KB  
Article
New Insights into CRISPR-like Arrays in Helicobacter pylori: An Exploratory Analysis from Genomic Data
by Paloma Camacho-Aguilar, Javier Alejandro Delgado-Nungaray, Eire Reynaga-Delgado, Orfil Gonzalez-Reynoso, Libia Zulema Rodriguez-Anaya, Luis Alfonso Muñoz Miranda, Gabriel Rincón Enríquez, Inocencio Higuera-Ciapara and Luis Joel Figueroa-Yáñez
Pathogens 2026, 15(5), 461; https://doi.org/10.3390/pathogens15050461 - 24 Apr 2026
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Abstract
Helicobacter pylori (H. pylori) is a highly adaptable gastric pathogen with marked genomic plasticity. Whilst functional CRISPR-Cas systems provide adaptive immunity in many bacteria, they have not been identified in H. pylori, unlike CRISPR-like sequences. In this study, eight H. [...] Read more.
Helicobacter pylori (H. pylori) is a highly adaptable gastric pathogen with marked genomic plasticity. Whilst functional CRISPR-Cas systems provide adaptive immunity in many bacteria, they have not been identified in H. pylori, unlike CRISPR-like sequences. In this study, eight H. pylori genomes were analysed using the bioinformatics tools CRISPRCasFinder, CRISPRCasTyper, and CRISPRloci. A total of 25 CRISPR-like arrays were identified, showing high conservation (88%) both between and within strains, suggesting that these arrays are not random remnants but rather organised structures possibly involved in cellular processes. Notably, a structural association was observed between the CRISPR-like sequences and the cag pathogenicity island (CagA-PAI). Conversely, CagA-PAI instability in specific strains was observed in the presence of the TnpA and TnpB transposons. Furthermore, in strain 29CaP, CRISPR-like assemblies were located in genomic proximity to the prophage Helico 1961P, leading to the hypothesis of a compensatory or regulatory effect in the absence of CagA-PAI. Taken together, these findings indicate that CRISPR-like arrays in H. pylori characterise a genomic architecture within regions of high plasticity. This study provides a solid exploratory foundation for future functional research on the adaptive and pathogenic evolution of H. pylori. Full article
(This article belongs to the Special Issue Pathogenesis, Antibiotic Resistance, and Host Immune Responses to Bacterial Infections)
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14 pages, 678 KB  
Article
Glnk Mediates Carbapenem Resistance Through the NtrB/NtrC-OprD Regulatory Pathway in Pseudomonas aeruginosa
by Xiaomeng Sun, Yiming Li, Xuetao Gong, Qitong Du, Yongxin Jin, Zhihui Cheng, Shouguang Jin and Weihui Wu
Pathogens 2026, 15(3), 289; https://doi.org/10.3390/pathogens15030289 - 6 Mar 2026
Viewed by 808
Abstract
Pseudomonas aeruginosa is a major causative agent of nosocomial infections worldwide. Carbapenems are the first-line agents for combating severe P. aeruginosa infections. However, the increasing prevalence of carbapenem-resistant P. aeruginosa (CRPA) has developed as a critical threat to global healthcare systems. In this [...] Read more.
Pseudomonas aeruginosa is a major causative agent of nosocomial infections worldwide. Carbapenems are the first-line agents for combating severe P. aeruginosa infections. However, the increasing prevalence of carbapenem-resistant P. aeruginosa (CRPA) has developed as a critical threat to global healthcare systems. In this study, we demonstrated that a mutation in the core nitrogen metabolism regulatory gene glnK decreases carbapenem resistance in P. aeruginosa. OprD, the major porin for carbapenem uptake, is upregulated in the glnK mutant, resulting in decreased resistance. We further found that the NtrB/NtrC two-component regulatory system is upregulated in the glnK mutant. An electrophoretic mobility shift assay (EMSA) and genetic studies revealed a direct regulatory role of NtrC on the expression of oprD. Deletion of ntrB, ntrC, or oprD in the glnK mutant restored the bacterial resistance to carbapenems. These results reveal that a GlnK-NtrB/NtrC-OprD regulatory pathway affects carbapenem resistance, shedding light on the regulatory relationship between nitrogen metabolism and carbapenem resistance in P. aeruginosa. Full article
(This article belongs to the Special Issue Pathogenesis, Antibiotic Resistance, and Host Immune Responses to Bacterial Infections)
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