Pseudogenization of the Secreted Effector Gene sseI Confers Rapid Systemic Dissemination of S. Typhimurium ST313 within Migratory Dendritic Cells

Carden, Sarah; Walker, G.; Honeycutt, Jared; Lugo, Kyler A.; Pham, Trung H.M.; Jacobson, Amanda; Bouley, Donna M.; Idoyaga, Juliana; Tsolis, Renée M.; Monack, Denise M.

doi:10.1016/j.chom.2017.01.009

Cited by 80 publications

(96 citation statements)

References 45 publications

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“…Reported to inhibit endosomal trafficking (Freeman, Rappl, Kuhle, Hensel, & Miller, 2002;Uchiya et al, 1999) SseI (SrfH) Bacteriophage (Gifsy-2) STM1051 Absent Absent Interacts with IQGAP1 resulting in inhibition of macrophage and dendritic cell migration (McLaughlin et al, 2009). Pseudogenisation promotes systemic dissemination (Carden et al, 2017) SseJ STM1631 t1534 a (STY1439) a…”

Section: Stm4157mentioning

confidence: 99%

TyphoidalSalmonella: Distinctive virulence factors and pathogenesis

Johnson

Mylona

Frankel

2018

Cellular Microbiology

136

106

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Although nontyphoidal Salmonella (NTS; including Salmonella Typhimurium) mainly cause gastroenteritis, typhoidal serovars (Salmonella Typhi and Salmonella Paratyphi A) cause typhoid fever, the treatment of which is threatened by increasing drug resistance. Our understanding of S. Typhi infection in human remains poorly understood, likely due to the host restriction of typhoidal strains and the subsequent popularity of the S. Typhimurium mouse typhoid model. However, translating findings with S. Typhimurium across to S. Typhi has some limitations. Notably, S. Typhi has specific virulence factors, including typhoid toxin and Vi antigen, involved in symptom development and immune evasion, respectively. In addition to unique virulence factors, both typhoidal and NTS rely on two pathogenicity-island encoded type III secretion systems (T3SS), the SPI-1 and SPI-2 T3SS, for invasion and intracellular replication. Marked differences have been observed in terms of T3SS regulation in response to bile, oxygen, and fever-like temperatures. Moreover, approximately half of effectors found in S. Typhimurium are either absent or pseudogenes in S. Typhi, with most of the remaining exhibiting sequence variation. Typhoidal-specific T3SS effectors have also been described. This review discusses what is known about the pathogenesis of typhoidal Salmonella with emphasis on unique behaviours and key differences when compared with S. Typhimurium.

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Section: Stm4157mentioning

confidence: 99%

TyphoidalSalmonella: Distinctive virulence factors and pathogenesis

Johnson

Mylona

Frankel

2018

Cellular Microbiology

136

106

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“…While genes encoding components of the type III secretion systems (T3SS) 1 and 2 apparatus were never HDCS, several genes encoding effector proteins secreted by them were (sseI, sseK2, sseK3, avrA, sseL, sseJ and gtgE). The sseI gene is inactivated in ST313 due to insertion of a transposable element, and results in hyper dissemination of these strains to systemic sites of the host via CD11b + migratory dendritic cells 46 . The sseK2, sseK3, avrA and sseL genes each encode effectors that inhibit the NFκB signalling pathway thereby modulating the proinflammatory response during infection [47][48][49] .…”

mentioning

confidence: 99%

Evolution of Salmonella enterica serotype Typhimurium driven by anthropogenic selection and niche adaptation

Bawn

Thilliez

Kirkwood

et al. 2019

Preprint

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Salmonella enterica serotype Typhimurium (S. Typhimurium) is a leading cause of gastroenteritis and disseminated disease worldwide, and a model organism for host pathogen interactions. Genotypic variation of S. Typhimurium results in strains with diverse host range, pathogenicity and risk to food safety. A robust fully parsimonious phylogenetic tree constructed from recombination purged variation in the whole genome sequence of 131 diverse strains of S. Typhimurium revealed population structure composed of two high order clades (α and β) and multiple subclades on extended internal branches, that exhibited distinct signatures of host adaptation and anthropogenic selection. Clade α contained a number of subclades composed of strains from well characterized epidemics in domesticated animals, while clade β predominantly contained subclades associated with wild avian species, with the notable exception of a subclade containing the DT204/49 complex. The contrasting epidemiology of α and β strains was reflected in distinct distribution of antimicrobial resistance (AMR) genes, accumulation of hypothetically disrupted coding sequences (HDCS), and signatures of functional diversification associated with invasiveness of host adapted serotypes. Gene flux was predominantly driven by acquisition, loss or recombination of prophage, awhile acquisition of large genetic islands (SGI-1 and 4) was restricted to two recent pandemic clones (DT104 and monophasic S. Typhimurium ST34) in clade α.Together, our data are consistent with the view that a broad host range common ancestor of S.Typhimurium diversified with clade α lineages remained largely associated with multiple domesticated animal species, while clade β spawned multiple lineages that underwent diversifying selection associated with adaptation to various niches, predominantly in wild avian species.

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“…For example, the T3SS/SPI-2 Salmonella secreted effector I (SseI) inhibits DC migration to the spleen which in turn impedes bacterial clearance [133]. Interestingly, a recent strain of iNTS, which is endemic to sub-Sarahan Africa, was recently shown to hyperdisseminate into systemic organs of mice, correlating with the natural pseudogenization of SseI, rendering this effector untranslatable during infection [134]. This ascribes a direct effect of the T3SS on bacterial dissemination through immune cell modulation.…”

Section: Salmonella Exploitation and Subversion Of The Immune Respmentioning

confidence: 99%

Salmonella infection: Interplay between the bacteria and host immune system

2017

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Salmonella infection causes morbidity and mortality throughout the world with the host immune response varying depending on whether the infection is acute and limited, or systemic and chronic. Additionally, Salmonella bacteria have evolved multiple mechanisms to avoid or subvert immunity to its own benefit and often the anatomical location of infection plays a role in both the immune response and bacterial fate. Here, we provide an overview of the interplay between the immune system and Salmonella, while discussing how different host and bacterial factors influence the outcome of infection.

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Pseudogenization of the Secreted Effector Gene sseI Confers Rapid Systemic Dissemination of S. Typhimurium ST313 within Migratory Dendritic Cells

Cited by 80 publications

References 45 publications

TyphoidalSalmonella: Distinctive virulence factors and pathogenesis

TyphoidalSalmonella: Distinctive virulence factors and pathogenesis

Evolution of Salmonella enterica serotype Typhimurium driven by anthropogenic selection and niche adaptation

Salmonella infection: Interplay between the bacteria and host immune system

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