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Bacterial Adaptive Strategies inside Host Cells

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: closed (30 June 2023) | Viewed by 2511

Special Issue Editor


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Guest Editor
Department of Pathobiology, University of Illinois at Urbana−Champaign, Urbana, IL 61802, USA
Interests: modulation of airway mucus hypersecretion by respiratory pathogens in chronic lung diseases; interaction of bacterial pathogens with alveolar epithelium during lung infection; regulation of genetic transfer and virulence by Streptococcus pneumoniae competence regulon during lung infection

Special Issue Information

Dear Colleagues,

It is well known that intracellular bacterial pathogens infect and persist inside their hosts. Additionally, facultative intracellular bacterial pathogens, as well as extracellular bacterial pathogens, also display phases in their infection cycles that require them to survive within host cells. Sensing of the host environments, such as temperature, pH, ionic strength, and host defense components, invading bacterial pathogens and opportunistic commensals elaborate survival mechanisms intracellularly, including the expression of factors required for invasion, evasion, proliferation and persistence. Many intracellular bacterial pathogens express factors which are similar to host proteins in order to mimic and co-opt host cellular processes to promote colonization and intracellular survival. Similarly, facultative intracellular pathogens such as Salmonella and Listeria species can invade and survive in phagocytic and non-phagocytic cells by the expression of virulence genes for invasion, survival and spread. Additionally, many extracellular pathogens, including Pseudomonas aeruginosa and Staphylococcus aureus, exhibit an initial intracellular phase of infection to hide from the host's immune system and antibiotics therapy, allowing them to persist and eventually switch to a typical extracellular infection. Finally, bacterial symbionts deliver factors into host cells that suppress immune defense, alter the gene expression, or modify host morphology or physiology that promote the nutrition and proliferation of the symbiont.

In this Special Issue, we invite the submission of original research articles, review articles and short communications covering human, animal, and plant bacterial pathogens in topics that include but not limited to the following: active immune suppression of the host cells by bacterial virulence factors, immune evasion by bacterial pathogens, molecular and cellular host mimicry and manipulation in bacterial symbionts, and modulation of survival mechanisms of persister cells in persistent infection.  Novel technological breakthroughs in early detection of infection by intracellular pathogens, as well as omics/computation approaches to examine the evolution of bacterial traits that promote intracellular survival are also welcome.

Prof. Dr. Gee Lau
Guest Editor

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Keywords

  • intracellular pathogens and facultative intracellular pathogens
  • host environment
  • bacterial survival mechanisms
  • host mimicry
  • host invasion, evasion and proliferation
  • bacterial persistence

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Published Papers (1 paper)

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Research

17 pages, 2587 KiB  
Article
YbdO Promotes the Pathogenicity of Escherichia coli K1 by Regulating Capsule Synthesis
by Yu Fan, Hongmin Sun, Wen Yang, Jing Bai, Peng Liu, Min Huang, Xi Guo, Bin Yang and Lu Feng
Int. J. Mol. Sci. 2022, 23(10), 5543; https://doi.org/10.3390/ijms23105543 - 16 May 2022
Cited by 4 | Viewed by 2111
Abstract
Escherichia coli K1 is the most popular neonatal meningitis-causing Gram-negative bacterium. As a key virulence determinant, the K1 capsule enhances the survival of E. coli K1 in human brain microvascular endothelial cells (HBMECs) upon crossing the blood–brain barrier; however, the regulatory mechanisms of [...] Read more.
Escherichia coli K1 is the most popular neonatal meningitis-causing Gram-negative bacterium. As a key virulence determinant, the K1 capsule enhances the survival of E. coli K1 in human brain microvascular endothelial cells (HBMECs) upon crossing the blood–brain barrier; however, the regulatory mechanisms of capsule synthesis during E. coli K1 invasion of HBMECs remain unclear. Here, we identified YbdO as a transcriptional regulator that promotes E. coli K1 invasion of HBMECs by directly activating K1 capsule gene expression to increase K1 capsule synthesis. We found that ybdO deletion significantly reduced HBMEC invasion by E. coli K1 and meningitis occurrence in mice. Additionally, electrophoretic mobility shift assay and chromatin immunoprecipitation–quantitative polymerase chain reaction analysis indicated that YbdO directly activates kpsMT and neuDBACES expression, which encode products involved in K1 capsule transport and synthesis by directly binding to the kpsM promoter. Furthermore, ybdO transcription was directly repressed by histone-like nucleoid structuring protein (H-NS), and we observed that acidic pH similar to that of early and late endosomes relieves this transcriptional repression. These findings demonstrated the regulatory mechanism of YbdO on K1 capsule synthesis, providing further insights into the evolution of E. coli K1 pathogenesis and host–pathogen interaction. Full article
(This article belongs to the Special Issue Bacterial Adaptive Strategies inside Host Cells)
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