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Focus on Bacterial Pathogens: Host Cell Defense Pathways and Innovative Therapeutic Strategies

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 4341

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Special Issue Editor

Prof. Dr. Edyta Juszczuk-Kubiak

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Guest Editor

Laboratory of Biotechnology and Molecular Engineering, Department of Microbiology, Prof. Wacław Dąbrowski Institute of Agricultural and Food Biotechnology—State Research Institute, 02-532 Warsaw, Poland
Interests: host bacterial pathogens; gut microbiota; metagenomics; host genomics; next-generation of probiotics (NGP) and psychobiotics; gut dysbiosis and host diseases; in vitro models of bacterial pathogens and gut epithelium interaction

Special Issue Information

Dear Colleagues,

Defence mechanisms play a crucial role in the host body, effectively preventing invasive microbial disease development. The innate system is the first line of defense including specific cells that synthesise different effector molecules to activate molecular mechanisms resulting in the elimination of pathogens. Despite the advancements in modern medicine, bacterial pathogens continue to pose one of the greatest risks to human health. The “Gold Age” of antibiotic application has led to an increase in the rapid development of multidrug-resistant (MDR) bacteria, leading to more difficult-to-treat infections. Therefore, infection by bacterial pathogens remains a significant health challenge worldwide. The emergence of MDR strains has further complicated treatment strategies, highlighting the need for innovative approaches to combat bacterial pathogens. The host immune response is crucial in controlling pathogen infections, and an understanding of the underlying mechanisms can lead to the development of innovative therapeutic strategies, opening up new avenues for the treatment and prevention of human and animal infections.

This Special Issue focuses on a comprehensive understanding of the host-cell defense mechanisms against bacterial pathogens and the development of novel therapeutic interventions to combat bacterial pathogens. I invite contributions from researchers, clinicians and other experts in the field to submit original research articles, reviews and perspectives on the above topics. I encourage submissions that emphasise novel therapeutic approaches and innovative strategies to improve the treatment outcomes of bacterial infections.

Prof. Dr. Edyta Juszczuk-Kubiak
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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 and virulence factors
host immune response to bacterial infection
innate and adaptive immunity against bacterial pathogens
immune evasion strategies employed by bacterial pathogens
innovative therapeutic strategies against bacterial pathogens
antimicrobial resistance and novel treatment strategies

Published Papers (3 papers)

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Research

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12 pages, 1806 KiB

Open AccessArticle

O26 Polysaccharides as Key Players in Enteropathogenic E. coli Immune Evasion and Vaccine Development

by Thiago Jordão da Silva Lemos, Herbert Guimarães de Sousa Silva, José Osvaldo Previato, Lucia Mendonça-Previato, Elisangela Oliveira de Freitas, Angela Silva Barbosa, Marcia Regina Franzolin, Luis Fernando dos Santos, Bruna de Sousa Melo, Geovana Ferreira dos Anjos, Renata Hiromi Nakagima Gonçalves and Marta de Oliveira Domingos

Int. J. Mol. Sci. 2024, 25(5), 2878; https://doi.org/10.3390/ijms25052878 - 1 Mar 2024

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Abstract

Enteropathogenic Escherichia coli (EPEC) produce a capsule of polysaccharides identical to those composing the O-antigen polysaccharide of its LPS (lipopolysaccharide) molecules. In light of this, the impact of O26 polysaccharides on the immune evasion mechanisms of capsulated O26 EPEC compared to non-capsulated enterohemorrhagic Escherichia coli (EHEC) was investigated. Our findings reveal that there was no significant difference between the levels in EPEC and EHEC of rhamnose (2.8:2.5), a molecule considered to be a PAMP (Pathogen Associated Molecular Patterns). However, the levels of glucose (10:1.69), heptose (3.6:0.89) and N-acetylglucosamine (4.5:2.10), were significantly higher in EPEC than EHEC, respectively. It was also observed that the presence of a capsule in EPEC inhibited the deposition of C3b on the bacterial surface and protected the pathogen against lysis by the complement system. In addition, the presence of a capsule also protected EPEC against phagocytosis by macrophages. However, the immune evasion provided by the capsule was overcome in the presence of anti-O26 polysaccharide antibodies, and additionally, these antibodies were able to inhibit O26 EPEC adhesion to human epithelial cells. Finally, the results indicate that O26 polysaccharides can generate an effective humoral immune response, making them promising antigens for the development of a vaccine against capsulated O26 E. coli. Full article

(This article belongs to the Special Issue Focus on Bacterial Pathogens: Host Cell Defense Pathways and Innovative Therapeutic Strategies)

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14 pages, 3644 KiB

Open AccessArticle

Baicalin Attenuates Panton–Valentine Leukocidin (PVL)-Induced Cytoskeleton Rearrangement via Regulating the RhoA/ROCK/LIMK and PI3K/AKT/GSK-3β Pathways in Bovine Mammary Epithelial Cells

by Jiangliu Yang, Zhenzhen Hai, Ling Hou, Yang Liu, Dongtao Zhang and Xuezhang Zhou

Int. J. Mol. Sci. 2023, 24(19), 14520; https://doi.org/10.3390/ijms241914520 - 25 Sep 2023

Cited by 1 | Viewed by 921

Abstract

Pore-forming toxins (PFTs) exert physiological effects by rearrangement of the host cell cytoskeleton. Staphylococcus aureus-secreted PFTs play an important role in bovine mastitis. In the study, we examined the effects of recombinant Panton–Valentine leukocidin (rPVL) on cytoskeleton rearrangement, and identified the signaling pathways involved in regulating the process in bovine mammary epithelial cells (BMECs) in vitro. Meanwhile, the underlying regulatory mechanism of baicalin for this process was investigated. The results showed that S. aureus induced cytoskeleton rearrangement in BMECs mainly through PVL. S. aureus and rPVL caused alterations in the cell morphology and layer integrity due to microfilament and microtubule rearrangement and focal contact inability. rPVL strongly induced the phosphorylation of cofilin at Ser3 mediating by the activation of the RhoA/ROCK/LIMK pathway, and resulted in the activation of loss of actin stress fibers, or the hyperphosphorylation of Tau at Ser396 inducing by the inhibition of the PI3K/AKT/GSK-3β pathways, and decreased the microtubule assembly. Baicalin significantly attenuated rPVL-stimulated cytoskeleton rearrangement in BMECs. Baicalin inhibited cofilin phosphorylation or Tau hyperphosphorylation via regulating the activation of RhoA/ROCK/LIMK and PI3K/AKT/GSK-3β signaling pathways. These findings provide new insights into the pathogenesis and potential treatment in S. aureus causing bovine mastitis. Full article

(This article belongs to the Special Issue Focus on Bacterial Pathogens: Host Cell Defense Pathways and Innovative Therapeutic Strategies)

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Review

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40 pages, 2225 KiB

Open AccessReview

Molecular Aspects of the Functioning of Pathogenic Bacteria Biofilm Based on Quorum Sensing (QS) Signal-Response System and Innovative Non-Antibiotic Strategies for Their Elimination

by Edyta Juszczuk-Kubiak

Int. J. Mol. Sci. 2024, 25(5), 2655; https://doi.org/10.3390/ijms25052655 - 24 Feb 2024

Viewed by 2346

Abstract

One of the key mechanisms enabling bacterial cells to create biofilms and regulate crucial life functions in a global and highly synchronized way is a bacterial communication system called quorum sensing (QS). QS is a bacterial cell-to-cell communication process that depends on the bacterial population density and is mediated by small signalling molecules called autoinducers (AIs). In bacteria, QS controls the biofilm formation through the global regulation of gene expression involved in the extracellular polymeric matrix (EPS) synthesis, virulence factor production, stress tolerance and metabolic adaptation. Forming biofilm is one of the crucial mechanisms of bacterial antimicrobial resistance (AMR). A common feature of human pathogens is the ability to form biofilm, which poses a serious medical issue due to their high susceptibility to traditional antibiotics. Because QS is associated with virulence and biofilm formation, there is a belief that inhibition of QS activity called quorum quenching (QQ) may provide alternative therapeutic methods for treating microbial infections. This review summarises recent progress in biofilm research, focusing on the mechanisms by which biofilms, especially those formed by pathogenic bacteria, become resistant to antibiotic treatment. Subsequently, a potential alternative approach to QS inhibition highlighting innovative non-antibiotic strategies to control AMR and biofilm formation of pathogenic bacteria has been discussed. Full article

(This article belongs to the Special Issue Focus on Bacterial Pathogens: Host Cell Defense Pathways and Innovative Therapeutic Strategies)

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