Functional analysis of type III secretion system 2 of Vibrio parahaemolyticus

SUMMARYPathogens utilize type III secretion systems to deliver effector proteins, which facilitate bacterial infections. The Escherichia coli type III secretion system 2 (ETT2) which plays a crucial role in bacterial virulence, is present in the majority of E. coli strains, although ETT2 has undergone widespread mutational attrition. We investigated the distribution and characteristics of ETT2 in avian pathogenic E. coli (APEC) isolates and identified five different ETT2 isoforms, including intact ETT2, in 57·6% (141/245) of the isolates. The ETT2 locus was present in the predominant APEC serotypes O78, O2 and O1. All of the ETT2 loci in the serotype O78 isolates were degenerate, whereas an intact ETT2 locus was mostly present in O1 and O2 serotype strains, which belong to phylogenetic groups B2 and D, respectively. Interestingly, a putative second type III secretion-associated locus (eip locus) was present only in the isolates with an intact ETT2. Moreover, ETT2 was more widely distributed in APEC isolates and exhibited more isoforms compared to ETT2 in human extraintestinal pathogenic E. coli, suggesting that APEC might be a potential risk to human health. However, there was no distinct correlation between ETT2 and other virulence factors in APEC.

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DctR contributes to the virulence of avian pathogenic Escherichia coli through regulation of type III secretion system 2 expression

Veterinary Research ◽

10.1186/s13567-021-00970-6 ◽

2021 ◽

Vol 52 (1) ◽

Author(s):

Yaodong Zhang ◽

Yao Wang ◽

Hong Zhu ◽

Zhengfei Yi ◽

Dossêh Jean Apôtre Afayibo ◽

...

Keyword(s):

Escherichia Coli ◽

Mutant Strain ◽

Type Iii Secretion ◽

Type Iii Secretion System ◽

Secretion System ◽

Economic Losses ◽

Type Iii ◽

Pathogenic Escherichia Coli ◽

Successful Infection ◽

System 2

AbstractPathogens could precisely alter their gene expression to facilitate their survival and successful infection. The LuxR family transcriptional regulator DctR (also known as YhiF) was shown to participate in the regulation of acid fitness and adhesion of enterohemorrhagic E. coli (EHEC) O157:H7. Avian pathogenic Escherichia coli (APEC) causes significant economic losses to the poultry industries and also potentially threatens human health. However, the effects of DctR on the fitness and virulence of APEC have not been investigated yet. To assess the function of DctR in APEC, the dctR gene mutant and complemented strains were constructed and biologically characterized. Our results show that inactivation of the dctR gene led to decreased biofilm formation, diminished serum resistance, reduced adherence capacity, attenuated colonization and virulence of APEC in ducks. The altered capacities of the mutant strain were restored by genetic complementation. In addition, we found that DctR positively regulates the expression of E. coli type III secretion system 2 (ETT2) core genes in APEC. The expression of the inflammatory cytokines interleukin (IL)-1β and IL-8 were decreased in HD-11 macrophages infected with the mutant strain compared with the wild-type strain. These observations indicate that regulator DctR contributes to the virulence of APEC through regulation of ETT2 expression.

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A Novel Phage Element of Salmonella enterica Serovar Enteritidis P125109 Contributes to Accelerated Type III Secretion System 2-Dependent Early Inflammation Kinetics in a Mouse Colitis Model

Infection and Immunity ◽

10.1128/iai.00180-12 ◽

2012 ◽

Vol 80 (9) ◽

pp. 3236-3246 ◽

Cited By ~ 22

Author(s):

Vikalp Vishwakarma ◽

Balamurugan Periaswamy ◽

Niladri Bhusan Pati ◽

Emma Slack ◽

Wolf-Dietrich Hardt ◽

...

Keyword(s):

Type Iii Secretion ◽

Salmonella Enterica ◽

Type Iii Secretion System ◽

Secretion System ◽

Pathogenic Potential ◽

Putative Gene ◽

Content Type ◽

Type Iii ◽

Genomic Study ◽

System 2

ABSTRACTSalmonella entericasubsp. I serovar Enteritidis exhibits type III secretion system 2 (TTSS2)-dependent early colonization and inflammation kinetics faster than those of closely relatedS. entericaserovar Typhimurium. To investigate the accelerated TTSS-2-dependent pathogenic potential ofS. Enteritidis, we focused on its genome. Results of a previously published comparative genomic study revealed the presence of mutually exclusive genes in both serovars. In this study, we investigated the roles of sixS. Enteritidis-specific genesin vivoby using differential fluorescence induction (DFI) through putative gene-specific promoters. The promoter construct associated with the gene locusSEN1140induced green fluorescent protein (GFP) expression in the gut lumen, lamina propria, mesenteric lymph nodes, and related systemic organs. To further investigate the potential role ofSEN1140, we compared aSEN1140deletion mutant withS. Typhimurium in a TTSS1-deficient background. Interestingly, theS. Enteritidis mutant lackingSEN1140did not show the unique TTSS-2-dependent early colonization and inflammation kinetic phenotype ofS. Typhimurium. Consistent with this result, complementation ofSEN1140restored the TTSS-2-dependent accelerated inflammatory potential ofS. Enteritidis. This report presents a suitable screening strategy that uses a combination of DFI, fluorescence-activated cell sorting, quantitative PCR, and wild-type isogenic tagged-strain techniques to explore the unique roles ofS. Enteritidis-specific genes in bacterial pathogenesis.

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