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Host-Pathogen Interactions during Persistent Bacterial Infections, 2nd Edition

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: 20 September 2025 | Viewed by 565

Special Issue Editor


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Guest Editor
Institute of Medical Microbiology, Jena University Hospital, Am Klinikum 1, D-07747 Jena, Germany
Interests: toxin-mediated effects in bacterial infections and viral-bacterial co-infections; persistence strategies of pathogens; infection models and testing of therapy strategies; diagnostic microbiology
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Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue “Host-Pathogen Interactions during Persistent Bacterial Infections” (https://www.mdpi.com/journal/ijms/special_issues/9MW6L7UFH9).

One of the main bacterial strategies during persistence is to manipulate the host response to promote microbial survival. Bacterial adaptation is frequently used by pathogens upon the transition from the free-living state to an intracellular environment. In this scenario, bacterial pathogens regulate their virulence factors, phenotype and metabolic pathways to persist silently for long periods of time. The microbes are able to establish a niche to avoid their eradication despite antimicrobials and immune response. However, the persisting pathogens can escape from their niche, regain full virulence and develop a new episode of an infection. Thus, the study of bacterial adaptation to the host plays an important role in the progress of disease from acute to chronic and relapse infections.

On the other hand, the host competes with bacteria for nutrients and survival. Thus, host cells adapt their metabolic pathways to activate the bacterial clearance. This type of interaction between host and pathogen determines the outcome of the infection.

This Special Issue is dedicated to understanding the mechanisms that take place during the bacterial switch from an aggressive virulent to a silent persisting phenotype. Furthermore, changes induced by pathogens on host cells that promote bacterial persistence should be taken into consideration. Reviews and research articles focusing on understanding the interchange between the different phenotypes by multiple approaches that include molecular and cell biology tools, advanced imaging tools and -omics techniques are welcome.

Prof. Dr. Bettina Löffler
Guest Editor

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Keywords

  • bacteria
  • intracellular adaptation
  • metabolic adaptation
  • metabolic host reprogramming
  • host–pathogen interaction
  • chronic infections
  • regulation of virulence

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Published Papers (1 paper)

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Research

16 pages, 5263 KiB  
Article
Colonizing Bacteria Aggravate Inflammation, Cytotoxicity and Immune Defense During Influenza A Virus Infection
by Liane Giebeler, Christina Ehrhardt, Antje Häder, Thurid Lauf, Stefanie Deinhardt-Emmer and Bettina Löffler
Int. J. Mol. Sci. 2025, 26(11), 5364; https://doi.org/10.3390/ijms26115364 - 3 Jun 2025
Viewed by 297
Abstract
A diverse bacterial community colonizes the respiratory system, including commensals such as Staphylococcus epidermidis (S. epidermidis) and Streptococcus salivarius (S. salivarius), as well as facultative pathogens like Staphylococcus aureus (S. aureus). This study aimed to establish a colonized cell culture model [...] Read more.
A diverse bacterial community colonizes the respiratory system, including commensals such as Staphylococcus epidermidis (S. epidermidis) and Streptococcus salivarius (S. salivarius), as well as facultative pathogens like Staphylococcus aureus (S. aureus). This study aimed to establish a colonized cell culture model to investigate the impact of these bacteria on influenza A virus (IAV) infection. Respiratory epithelial cells were exposed to S. epidermidis, S. salivarius, or S. aureus, using either live or heat-inactivated bacteria, followed by IAV infection. Cell integrity was assessed microscopically, cytotoxicity was measured via LDH assay, and inflammatory responses were analyzed through cytokine expression. Additionally, macrophage function was examined in response to bacterial colonization and IAV infection. While commensals maintained epithelial integrity for 48 h, S. aureus induced severe cell damage and death. The most pronounced epithelial destruction was caused by coinfection with S. aureus and IAV. Notably, commensals did not confer protection against IAV but instead enhanced epithelial inflammation. These effects were dependent on live bacteria, as inactivated bacteria had no impact. However, prior exposure to S. epidermidis and S. salivarius improved macrophage-mediated immune responses against IAV. These findings suggest that while individual commensals do not directly protect epithelial cells, they may contribute to immune training and enhance lung defense mechanisms. Full article
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