Type III Secretion Systems in Human/Animal Pathogenic Bacteria 2.0

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Molecular Microbiology and Immunology".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 13544

Special Issue Editors


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Guest Editor
Departamento de Genética, Facultad de Biología, Universidad de Sevilla, Sevilla, Spain
Interests: Salmonella; host–pathogen interaction; type III secretion; signal transduction; gene regulation
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Guest Editor
Genetics Department, University of Seville, Sevilla, Spain
Interests: Salmonella; host–pathogen interaction; type III secretion; biofilms; zebrafish
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Type III secretion systems (T3SS) were discovered in the 1990s and initially described in the animal pathogen Yersinia, but they are present in many Gram-negative bacterial pathogens and symbionts of animal and plants. These systems are important virulence factors for many animal pathogenic bacteria and consist of a needle-like structure that spans inner and outer bacterial membranes and the host cell membrane to deliver effector proteins into the host cytosol. These effectors interfere with cellular functions to manipulate the host cells processes to benefit the pathogen.

Bacterial pathogens that use T3SS to communicate with host cells represent a major threat to human health and cause a broad spectrum of diseases and clinical manifestations. They include species of Shigella, Salmonella, Yersinia, Bordetella, Chlamydia, and Burkholderia, as well as enteropathogenic and enterohemorrhagic E. coli, and the opportunistic pathogen Pseudomonas aeruginosa. Some of them, together with species of Aeromonas, Citrobacter, Edwarsiella, Photorhabdus, or Vibrio, among others, can also cause infections in livestock and fisheries, leading to huge economic losses and, in some cases, increasing the risk of human infections.

In spite of the variety of lifestyles and diseases caused by these pathogens, there are also common themes arising from the fact that they share the use of T3SSs as key virulence mechanisms, and that effectors from different bacteria may have similar designs, biochemical activities, and/or functions. Therefore, researchers working in a particular T3SS can benefit from the studies carried out in other bacteria. Finally, these systems provide an opportunity to develop novel therapeutic approaches to respond to the growing number of antimicrobial-resistant pathogens, one of the ten threats to global health identified by the World Health Organization for this year.

This Special Issue focuses on the study of type III secretion systems in animal pathogenic bacteria and will publish high-quality research articles and reviews concerning this subject. We aim to address all aspects related to this topic, including: regulation of the expression of type III secretion systems and their effectors; mechanisms of type III protein secretion; conditions for secretion and translocation of effectors; host–pathogen specificity; structural studies; enzymatic activities, substrates, and interacting partners of the effectors; functional effects on the host; and biotechnological and biomedical applications.

Prof. Dr. Francisco Ramos-Morales
Dr. Joaquín Bernal-Bayard
Guest Editors

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Keywords

  • type III secretion
  • effectors
  • virulence
  • host-pathogen interactions
  • Aeromonas
  • Bordetella
  • Burkholderia
  • Chlamydia
  • Citrobacter
  • Edwardsiella
  • EPEC/EHEC
  • Photorhabdus
  • Pseudomonas
  • Salmonella
  • Shigella
  • Vibrio
  • Yersinia

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Published Papers (4 papers)

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Research

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14 pages, 2183 KiB  
Article
RyhB Paralogs Downregulate the Expressions of Multiple Survival-Associated Genes and Attenuate the Survival of Salmonella Enteritidis in the Chicken Macrophage HD11
by Xia Meng, Mengping He, Binjie Chen, Pengpeng Xia, Jinqiu Wang, Chunhong Zhu, Heng Wang and Guoqiang Zhu
Microorganisms 2023, 11(1), 214; https://doi.org/10.3390/microorganisms11010214 - 15 Jan 2023
Cited by 1 | Viewed by 2203
Abstract
RyhB-1 and RyhB-2 are small non-coding RNAs in Salmonella that act as regulators of iron homeostasis by sensing the environmental iron concentration. Expressions of RyhB paralogs from Salmonella Typhimurium are increased within microphages. RyhB paralogs restrain the growth of S. Typhimurium in RAW264.7 [...] Read more.
RyhB-1 and RyhB-2 are small non-coding RNAs in Salmonella that act as regulators of iron homeostasis by sensing the environmental iron concentration. Expressions of RyhB paralogs from Salmonella Typhimurium are increased within microphages. RyhB paralogs restrain the growth of S. Typhimurium in RAW264.7 macrophages by modulating the expression of Salmonella pathogenicity island 1 (SPI-1) genes sicA and rtsB. However, little is known about the regulatory role of RyhBs and their virulence-associated targets in Salmonella Enteritidis. We studied candidate targets of RyhB paralogs via RNA-Seq in conditions of iron limitation and hypoxia. RyhB paralogs were expressed when the S. Enteritidis strain CMCC(B)50336 (SE50336) interacted with the chicken macrophage line HD11. We analyzed gene expression associated with Salmonella survival and replication in macrophages in wild-type strain SE50336 and the RyhB deletion mutants after co-incubation with HD11 and screened out targets regulated by RyhBs. The expressions of both RyhB-1 and RyhB-2 were increased after co-incubation with HD11 for 8 h and several survival-associated genes within macrophages, such as ssaI, sseA, pagC, sodC, mgtC, yaeB, pocR, and hns, were upregulated in the ryhB-1 deletion mutant. Specifically, ssaI, the type-three secretion system 2 (T3SS-2) effector encoded by SPI-2, which promoted the survival of Salmonella in macrophages, was upregulated more than 3-fold in the ryhB-1 deletion mutant. We confirmed that both RyhB-1 and RyhB-2 downregulated the expression of ssaI to repress its mRNA translation by directly interacting with its coding sequence (CDS) region via an incomplete complementary base-pairing mechanism. The SPI-2 gene sseA was indirectly modulated by RyhB-1. The survival assays in macrophages showed that the ability of intracellular survival of ryhB-1 and/or ryhB-2 deletion mutants in HD11 was higher than that of the wild-type strain. These results indicate that RyhB paralogs downregulate survival-related virulence factors and attenuate the survival of S. Enteritidis inside chicken macrophage HD11. Full article
(This article belongs to the Special Issue Type III Secretion Systems in Human/Animal Pathogenic Bacteria 2.0)
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25 pages, 15048 KiB  
Article
CesL Regulates Type III Secretion Substrate Specificity of the Enteropathogenic E. coli Injectisome
by Miguel Díaz-Guerrero, Meztlli O. Gaytán, Eduardo Soto, Norma Espinosa, Elizabeth García-Gómez, Arely Marcos-Vilchis, Angel Andrade and Bertha González-Pedrajo
Microorganisms 2021, 9(5), 1047; https://doi.org/10.3390/microorganisms9051047 - 13 May 2021
Cited by 5 | Viewed by 2986
Abstract
The type III secretion system (T3SS) is a complex molecular device used by several pathogenic bacteria to translocate effector proteins directly into eukaryotic host cells. One remarkable feature of the T3SS is its ability to secrete different categories of proteins in a hierarchical [...] Read more.
The type III secretion system (T3SS) is a complex molecular device used by several pathogenic bacteria to translocate effector proteins directly into eukaryotic host cells. One remarkable feature of the T3SS is its ability to secrete different categories of proteins in a hierarchical manner, to ensure proper assembly and timely delivery of effectors into target cells. In enteropathogenic Escherichia coli, the substrate specificity switch from translocator to effector secretion is regulated by a gatekeeper complex composed of SepL, SepD, and CesL proteins. Here, we report a characterization of the CesL protein using biochemical and genetic approaches. We investigated discrepancies in the phenotype among different cesL deletion mutants and showed that CesL is indeed essential for translocator secretion and to prevent premature effector secretion. We also demonstrated that CesL engages in pairwise interactions with both SepL and SepD. Furthermore, while association of SepL to the membrane does not depended on CesL, the absence of any of the proteins forming the heterotrimeric complex compromised the intracellular stability of each component. In addition, we found that CesL interacts with the cytoplasmic domains of the export gate components EscU and EscV. We propose a mechanism for substrate secretion regulation governed by the SepL/SepD/CesL complex. Full article
(This article belongs to the Special Issue Type III Secretion Systems in Human/Animal Pathogenic Bacteria 2.0)
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Review

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0 pages, 2299 KiB  
Review
A Tale about Shigella: Evolution, Plasmid, and Virulence
by Nathaline Haidar-Ahmad, France Ourida Manigat, Navoun Silué, Stéphanie M. Pontier and François-Xavier Campbell-Valois
Microorganisms 2023, 11(7), 1709; https://doi.org/10.3390/microorganisms11071709 - 30 Jun 2023
Cited by 1 | Viewed by 3057
Abstract
Shigella spp. cause hundreds of millions of intestinal infections each year. They target the mucosa of the human colon and are an important model of intracellular bacterial pathogenesis. Shigella is a pathovar of Escherichia coli that is characterized by the presence of a [...] Read more.
Shigella spp. cause hundreds of millions of intestinal infections each year. They target the mucosa of the human colon and are an important model of intracellular bacterial pathogenesis. Shigella is a pathovar of Escherichia coli that is characterized by the presence of a large invasion plasmid, pINV, which encodes the characteristic type III secretion system and icsA used for cytosol invasion and cell-to-cell spread, respectively. First, we review recent advances in the genetic aspects of Shigella, shedding light on its evolutionary history within the E. coli lineage and its relationship to the acquisition of pINV. We then discuss recent insights into the processes that allow for the maintenance of pINV. Finally, we describe the role of the transcription activators VirF, VirB, and MxiE in the major virulence gene regulatory cascades that control the expression of the type III secretion system and icsA. This provides an opportunity to examine the interplay between these pINV-encoded transcriptional activators and numerous chromosome-encoded factors that modulate their activity. Finally, we discuss novel chromosomal genes icaR, icaT, and yccE that are regulated by MxiE. This review emphasizes the notion that Shigella and E. coli have walked the fine line between commensalism and pathogenesis for much of their history. Full article
(This article belongs to the Special Issue Type III Secretion Systems in Human/Animal Pathogenic Bacteria 2.0)
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22 pages, 3931 KiB  
Review
Recent Advancements in Tracking Bacterial Effector Protein Translocation
by Julie Braet, Dominiek Catteeuw and Petra Van Damme
Microorganisms 2022, 10(2), 260; https://doi.org/10.3390/microorganisms10020260 - 24 Jan 2022
Cited by 7 | Viewed by 4327
Abstract
Bacteria-host interactions are characterized by the delivery of bacterial virulence factors, i.e., effectors, into host cells where they counteract host immunity and exploit host responses allowing bacterial survival and spreading. These effectors are translocated into host cells by means of dedicated secretion systems [...] Read more.
Bacteria-host interactions are characterized by the delivery of bacterial virulence factors, i.e., effectors, into host cells where they counteract host immunity and exploit host responses allowing bacterial survival and spreading. These effectors are translocated into host cells by means of dedicated secretion systems such as the type 3 secretion system (T3SS). A comprehensive understanding of effector translocation in a spatio-temporal manner is of critical importance to gain insights into an effector’s mode of action. Various approaches have been developed to understand timing and order of effector translocation, quantities of translocated effectors and their subcellular localization upon translocation into host cells. Recently, the existing toolset has been expanded by newly developed state-of-the art methods to monitor bacterial effector translocation and dynamics. In this review, we elaborate on reported methods and discuss recent advances and shortcomings in this area of tracking bacterial effector translocation. Full article
(This article belongs to the Special Issue Type III Secretion Systems in Human/Animal Pathogenic Bacteria 2.0)
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