scholarly journals In the Absence of Effector Proteins, the Pseudomonas aeruginosa Type Three Secretion System Needle Tip Complex Contributes to Lung Injury and Systemic Inflammatory Responses

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e81792 ◽  
Author(s):  
Jonathon P. Audia ◽  
Ashley S. Lindsey ◽  
Nicole A. Housley ◽  
Courtney R. Ochoa ◽  
Chun Zhou ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Lung Injury ◽  
Inflammatory Responses ◽  
Secretion System ◽  
Effector Proteins ◽  
Type Three Secretion System ◽  
Type Three Secretion

The Type Three Secretion System of Pseudomonas aeruginosa as a Target for Development of Antivirulence Drugs

2020 ◽  
Vol 35 (1) ◽  
pp. 1-13
Author(s):  
A. B. Sheremet ◽  
L. N. Nesterenko ◽  
N. A. Zigangirova
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Secretion System ◽  
Type Three Secretion System ◽  
Type Three Secretion

scholarly journals Regulation of the Locus of Enterocyte Effacement in Attaching and Effacing Pathogens

2017 ◽  
Vol 200 (2) ◽  
Author(s):  
R. Christopher D. Furniss ◽  
Abigail Clements
Keyword(s):  
Secretion System ◽  
Effector Proteins ◽  
The Core ◽  
Genetic Feature ◽  
Gut Epithelium ◽  
Type Three Secretion System ◽  
Gut Mucosa ◽  
Enterocyte Effacement ◽  
Type Three Secretion ◽  
Complex Regulatory Network

ABSTRACTAttaching and effacing (AE) pathogens colonize the gut mucosa using a type three secretion system (T3SS) and a suite of effector proteins. The locus of enterocyte effacement (LEE) is the defining genetic feature of the AE pathogens, encoding the T3SS and the core effector proteins necessary for pathogenesis. Extensive research has revealed a complex regulatory network that senses and responds to a myriad of host- and microbiota-derived signals in the infected gut to control transcription of the LEE. These signals include microbiota-liberated sugars and metabolites in the gut lumen, molecular oxygen at the gut epithelium, and host hormones. Recent research has revealed that AE pathogens also recognize physical signals, such as attachment to the epithelium, and that the act of effector translocation remodels gene expression in infecting bacteria. In this review, we summarize our knowledge to date and present an integrated view of how chemical, geographical, and physical cues regulate the virulence program of AE pathogens during infection.

scholarly journals Chemical Inhibitors of the Type Three Secretion System: Disarming Bacterial Pathogens

2012 ◽  
Vol 56 (11) ◽  
pp. 5433-5441 ◽  
Author(s):  
Miles C. Duncan ◽  
Roger G. Linington ◽  
Victoria Auerbuch
Keyword(s):  
Bacterial Infections ◽  
Pathogenic Bacteria ◽  
Bacterial Pathogens ◽  
Secretion System ◽  
Effector Proteins ◽  
Host Cells ◽  
Magic Bullet ◽  
Antimicrobial Drugs ◽  
Type Three Secretion System ◽  
Type Three Secretion

ABSTRACTThe recent and dramatic rise of antibiotic resistance among bacterial pathogens underlies the fear that standard treatments for infectious disease will soon be largely ineffective. Resistance has evolved against nearly every clinically used antibiotic, and in the near future, we may be hard-pressed to treat bacterial infections previously conquered by “magic bullet” drugs. While traditional antibiotics kill or slow bacterial growth, an important emerging strategy to combat pathogens seeks to block the ability of bacteria to harm the host by inhibiting bacterial virulence factors. One such virulence factor, the type three secretion system (T3SS), is found in over two dozen Gram-negative pathogens and functions by injecting effector proteins directly into the cytosol of host cells. Without T3SSs, many pathogenic bacteria are unable to cause disease, making the T3SS an attractive target for novel antimicrobial drugs. Interdisciplinary efforts between chemists and microbiologists have yielded several T3SS inhibitors, including the relatively well-studied salicylidene acylhydrazides. This review highlights the discovery and characterization of T3SS inhibitors in the primary literature over the past 10 years and discusses the future of these drugs as both research tools and a new class of therapeutic agents.

scholarly journals Salmonella Pathogenicity Island 1 (SPI-1): The Evolution and Stabilization of a Core Genomic Type Three Secretion System

2020 ◽  
Vol 8 (4) ◽  
pp. 576
Author(s):  
Nicole A. Lerminiaux ◽  
Keith D. MacKenzie ◽  
Andrew D. S. Cameron
Keyword(s):  
Transcription Factors ◽  
Pathogenicity Island ◽  
Secretion System ◽  
Effector Proteins ◽  
Gene Promoters ◽  
Salmonella Pathogenicity Island ◽  
Evolutionary Origins ◽  
Type Three Secretion System ◽  
History Of ◽  
Type Three Secretion

Salmonella Pathogenicity Island 1 (SPI-1) encodes a type three secretion system (T3SS), effector proteins, and associated transcription factors that together enable invasion of epithelial cells in animal intestines. The horizontal acquisition of SPI-1 by the common ancestor of all Salmonella is considered a prime example of how gene islands potentiate the emergence of new pathogens with expanded niche ranges. However, the evolutionary history of SPI-1 has attracted little attention. Here, we apply phylogenetic comparisons across the family Enterobacteriaceae to examine the history of SPI-1, improving the resolution of its boundaries and unique architecture by identifying its composite gene modules. SPI-1 is located between the core genes fhlA and mutS, a hotspot for the gain and loss of horizontally acquired genes. Despite the plasticity of this locus, SPI-1 demonstrates stable residency of many tens of millions of years in a host genome, unlike short-lived homologous T3SS and effector islands including Escherichia ETT2, Yersinia YSA, Pantoea PSI-2, Sodalis SSR2, and Chromobacterium CPI-1. SPI-1 employs a unique series of regulatory switches, starting with the dedicated transcription factors HilC and HilD, and flowing through the central SPI-1 regulator HilA. HilA is shared with other T3SS, but HilC and HilD may have their evolutionary origins in Salmonella. The hilA, hilC, and hilD gene promoters are the most AT-rich DNA in SPI-1, placing them under tight control by the transcriptional repressor H-NS. In all Salmonella lineages, these three promoters resist amelioration towards the genomic average, ensuring strong repression by H-NS. Hence, early development of a robust and well-integrated regulatory network may explain the evolutionary stability of SPI-1 compared to T3SS gene islands in other species.

Targeting the Type Three Secretion System in Pseudomonas aeruginosa

2016 ◽  
Vol 37 (9) ◽  
pp. 734-749 ◽  
Author(s):  
Ahalieyah Anantharajah ◽  
Marie-Paule Mingeot-Leclercq ◽  
Françoise Van Bambeke
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Secretion System ◽  
Type Three Secretion System ◽  
Type Three Secretion

scholarly journals Structural and Functional Characterization of the Type Three Secretion System (T3SS) Needle of Pseudomonas aeruginosa

2019 ◽  
Vol 10 ◽  
Author(s):  
Charlotte Lombardi ◽  
James Tolchard ◽  
Stephanie Bouillot ◽  
Luca Signor ◽  
Caroline Gebus ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Functional Characterization ◽  
Secretion System ◽  
Type Three Secretion System ◽  
Type Three Secretion

scholarly journals Arginine glycosylation enhances methylglyoxal detoxification

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Samir El Qaidi ◽  
Nichollas E. Scott ◽  
Philip R. Hardwidge
Keyword(s):  
Secretion System ◽  
Effector Proteins ◽  
Glutathione Synthetase ◽  
Synthetase Activity ◽  
Host Cell Proteins ◽  
T3ss Effector ◽  
Type Three Secretion System ◽  
Arginine Residues ◽  
Host Signaling ◽  
Type Three Secretion

AbstractType III secretion system effector proteins have primarily been characterized for their interactions with host cell proteins and their ability to disrupt host signaling pathways. We are testing the hypothesis that some effectors are active within the bacterium, where they modulate bacterial signal transduction and physiology. We previously determined that the Citrobacter rodentium effector NleB possesses an intra-bacterial glycosyltransferase activity that increases glutathione synthetase activity to protect the bacterium from oxidative stress. Here we investigated the potential intra-bacterial activities of NleB orthologs in Salmonella enterica and found that SseK1 and SseK3 mediate resistance to methylglyoxal. SseK1 glycosylates specific arginine residues on four proteins involved in methylglyoxal detoxification, namely GloA (R9), GloB (R190), GloC (R160), and YajL (R149). SseK1-mediated Arg-glycosylation of these four proteins significantly enhances their catalytic activity, thus providing another important example of the intra-bacterial activities of type three secretion system effector proteins. These data are also the first demonstration that a Salmonella T3SS effector is active within the bacterium.

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