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Bacterial Adaptation Strategies to the Host: From Acute, Aggressive to Chronic, Dormant 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 February 2025 | Viewed by 3264

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 “Bacterial Adaptation Strategies to the Host: From Acute, Aggressive to Chronic, Dormant Infections”.

Host-pathogen interaction is highly dynamic and can turn in aggressive, tissue destructive diseases or only harmless colonization. In this interaction, the microbes employ several strategies to attack the host and establish an infection and at the same time to survive within hosts and enable their long term survival. The microbial flexibility to be adapted to several environments is directly linked to bacterial fitness. To establish an infection microbes produce a lot of virulence factors to damage host cells, to enter deep tissue structures and get nutrients for their growth. However, this aggressive microbial behaviour awake the immune host response which try to eliminate the microbial population. During the infection process, the microbes can switch to a dormant or metabolically less-active phenotypes to enhance their survival. Thus, the chronic phase of infection is defined as an intrinsic relationship between microbes and host where the microbe have a niche to be hidden from antimicrobials and immune response.

Bacteria turn to dormant or sleeping bacterial phenotypes when the nutrients are limited and allow them to save energy in this hostile environment. Sleeping bacterial phenotypes represent a big challenge to physicians because they are tolerant to several antimicrobials that require actively dividing bacterial cells. Furthermore, dormant bacteria can turn to active and aggressive phenotype when new nutrient sources are available, representing a potential risk for developing a new infection.

This switch from aggressive to dormant bacterial phenotype depends on the expression of virulence factors driven by a fine regulatory network and plays an important role in the progress of infection from acute to chronic phase.

This special issue is dedicated to understand the mechanisms that enable bacteria to turn from aggressive to dormant phenotypes that influence the outcome of the infection. Reviews and research articles focusing on understanding the interchange between active/aggressive to chronic dormant bacterial phenotype 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

  • dormancy
  • phenotype switching
  • bacterial stress
  • survival strategies
  • persisters
  • resuscitation
  • starvation
  • cell cycle arrest
  • ATP homeostasis

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Published Papers (2 papers)

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Research

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13 pages, 2315 KiB  
Article
The Controversial Effect of Antibiotics on Methicillin-Sensitive S. aureus: A Comparative In Vitro Study
by Valeria C. J. Hackemann, Stefan Hagel, Klaus D. Jandt, Jürgen Rödel, Bettina Löffler and Lorena Tuchscherr
Int. J. Mol. Sci. 2023, 24(22), 16308; https://doi.org/10.3390/ijms242216308 - 14 Nov 2023
Cited by 1 | Viewed by 1515
Abstract
Methicillin-sensitive Staphylococcus (S.) aureus (MSSA) bacteremia remains a global challenge, despite the availability of antibiotics. Primary treatments include β-lactam agents such as cefazolin and flucloxacillin. Ongoing discussions have focused on the potential synergistic effects of combining these agents with rifampicin or [...] Read more.
Methicillin-sensitive Staphylococcus (S.) aureus (MSSA) bacteremia remains a global challenge, despite the availability of antibiotics. Primary treatments include β-lactam agents such as cefazolin and flucloxacillin. Ongoing discussions have focused on the potential synergistic effects of combining these agents with rifampicin or fosfomycin to combat infections associated with biofilm formation. Managing staphylococcal infections is challenging due to antibacterial resistance, biofilms, and S. aureus’s ability to invade and replicate within host cells. Intracellular invasion shields the bacteria from antibacterial agents and the immune system, often leading to incomplete bacterial clearance and chronic infections. Additionally, S. aureus can assume a dormant phenotype, known as the small colony variant (SCV), further complicating eradication and promoting persistence. This study investigated the impact of antibiotic combinations on the persistence of S. aureus 6850 and its stable small colony variant (SCV strain JB1) focusing on intracellular survival and biofilm formation. The results from the wild-type strain 6850 demonstrate that β-lactams combined with RIF effectively eliminated biofilms and intracellular bacteria but tend to select for SCVs in planktonic culture and host cells. Higher antibiotic concentrations were associated with an increase in the zeta potential of S. aureus, suggesting reduced membrane permeability to antimicrobials. When using the stable SCV mutant strain JB1, antibiotic combinations with rifampicin successfully cleared planktonic bacteria and biofilms but failed to eradicate intracellular bacteria. Given these findings, it is reasonable to report that β-lactams combined with rifampicin represent the optimal treatment for MSSA bacteremia. However, caution is warranted when employing this treatment over an extended period, as it may elevate the risk of selecting for small colony variants (SCVs) and, consequently, promoting bacterial persistence. Full article
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Review

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11 pages, 1563 KiB  
Review
Trained Immunity and Trained Tolerance: The Case of Helicobacter pylori Infection
by Maria Pina Dore and Giovanni Mario Pes
Int. J. Mol. Sci. 2024, 25(11), 5856; https://doi.org/10.3390/ijms25115856 - 28 May 2024
Viewed by 1437
Abstract
Trained immunity is a concept in immunology in which innate immune cells, such as monocytes and macrophages, exhibit enhanced responsiveness and memory-like characteristics following initial contact with a pathogenic stimulus that may promote a more effective immune defense following subsequent contact with the [...] Read more.
Trained immunity is a concept in immunology in which innate immune cells, such as monocytes and macrophages, exhibit enhanced responsiveness and memory-like characteristics following initial contact with a pathogenic stimulus that may promote a more effective immune defense following subsequent contact with the same pathogen. Helicobacter pylori, a bacterium that colonizes the stomach lining, is etiologically associated with various gastrointestinal diseases, including gastritis, peptic ulcer, gastric adenocarcinoma, MALT lymphoma, and extra gastric disorders. It has been demonstrated that repeated exposure to H. pylori can induce trained immunity in the innate immune cells of the gastric mucosa, which become more responsive and better able to respond to subsequent H. pylori infections. However, interactions between H. pylori and trained immunity are intricate and produce both beneficial and detrimental effects. H. pylori infection is characterized histologically as the presence of both an acute and chronic inflammatory response called acute-on-chronic inflammation, or gastritis. The clinical outcomes of ongoing inflammation include intestinal metaplasia, gastric atrophy, and dysplasia. These same mechanisms may also reduce immunotolerance and trigger autoimmune pathologies in the host. This review focuses on the relationship between trained immunity and H. pylori and underscores the dynamic interplay between the immune system and the pathogen in the context of gastric colonization and inflammation. Full article
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