Functional dissection of translocon proteins of the Salmonella Pathogenicity Island 2-encoded type III secretion system

Hölzer, Stefanie U.; Hensel, Michael

doi:10.1186/1471-2180-10-104

Cited by 16 publications

(12 citation statements)

References 32 publications

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“…Deleting a single gene, such as eseB, eseD, escA, escC, or esaN, increased the 50% lethal dose (LD 50 ) by approximately 1 log in blue gourami fish (16)(17)(18). EseB, EseC, and EseD are homologous to SseB, SseC, and SseD of the Salmonella pathogenicity island 2 (SPI-2) T3SS, which are involved in the translocation of effectors (6,19,20). EscA is the chaperon of EseC (17), EscC is the chaperon of EseB and EseD (16), and EscB is the chaperon of EseG (18).…”

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confidence: 99%

Identification and Functional Characterization of the Novel Edwardsiella tarda Effector EseJ

et al. 2015

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e Edwardsiella tarda is a Gram-negative enteric pathogen that causes hemorrhagic septicemia in fish and gastro-and extraintestinal infections in humans. The type III secretion system (T3SS) of E. tarda has been identified as a key virulence factor that contributes to pathogenesis in fish. However, little is known about the associated effectors translocated by this T3SS. In this study, by comparing the profile of secreted proteins of the wild-type PPD130/91 and its T3SS ATPase ⌬esaN mutant, we identified a new effector by matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry. This effector consists of 1,359 amino acids, sharing high sequence similarity with Orf29/30 of E. tarda strain EIB202, and is renamed EseJ. The secretion and translocation of EseJ depend on the T3SS. A ⌬eseJ mutant strain adheres to epithelioma papillosum of carp (EPC) cells 3 to 5 times more extensively than the wild-type strain does. EseJ inhibits bacterial adhesion to EPC cells from within bacterial cells. Importantly, the ⌬eseJ mutant strain does not replicate efficiently in EPC cells and fails to replicate in J774A.1 macrophages. In infected J774A.1 macrophages, the ⌬eseJ mutant elicits higher production of reactive oxygen species than wild-type E. tarda. The replication defect is consistent with the attenuation of the ⌬eseJ mutant in the blue gourami fish model: the 50% lethal dose (LD 50 ) of the ⌬eseJ mutant is 2.34 times greater than that of the wild type, and the ⌬eseJ mutant is less competitive than the wild type in mixed infection. Thus, EseJ represents a novel effector that contributes to virulence by reducing bacterial adhesion to EPC cells and facilitating intracellular bacterial replication.

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confidence: 99%

Identification and Functional Characterization of the Novel Edwardsiella tarda Effector EseJ

et al. 2015

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“…Although no differences in body and spleen weight were found between Salmonella and Salmonella + MenSCs experimental groups, the bacterial load in MenSCs-injected mice increased remarkably in the spleen compared to the Salmonella group indicating significantly inferior bacteria clearance ( Fig. 3h, see Table S1) and suggesting an increment in the proliferative activity of the bacteria 35,37 . This pattern was also observed for peritoneal fluid and mesenteric nodes ( Fig.…”

Section: Resultsmentioning

confidence: 91%

Menstrual blood-derived stromal cells modulate functional properties of mouse and human macrophages

Aguilar

Romero-Pinedo

Ruiz-Magaña

et al. 2020

Sci Rep

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Menstrual blood-derived stromal cells (MenSCs) are emerging as a strong candidate for cell-based therapies due to their immunomodulatory properties. However, their direct impact on innate immune populations remains elusive. Since macrophages play a key role in the onset and development of inflammation, understanding MenSCs implication in the functional properties of these cells is required to refine their clinical effects during the treatment of inflammatory disorders. In this study, we assessed the effects that MenSCs had on the recruitment of macrophages and other innate immune cells in two mouse models of acute inflammation, a thioglycollate (TGC)-elicited peritonitis model and a monobacterial sepsis model. We found that, in the TGC model, MenSCs injection reduced the percentage of macrophages recruited to the peritoneum and promoted the generation of peritoneal immune cell aggregates. In the sepsis model, MenSCs exacerbated infection by diminishing the recruitment of macrophages and neutrophils to the site of infection and inducing defective bacterial clearance. Additional in vitro studies confirmed that co-culture with MenSCs impaired macrophage bactericidal properties, affecting bacterial killing and the production of reactive oxygen intermediates. Our findings suggest that MenSCs modulate the macrophage population and that this modulation must be taken into consideration when it comes to future clinical applications.

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“…To test this, we created a complementation strain (ΔeseC/pACYC-eseC-2HA) where a two-hemagglutinin (HA) tag was added at the C terminus of EseC. It is well known that certain genetic modifications at the C terminus of translocon proteins (such as SseB and SseD) tend to prevent the secretion of these proteins by the T3SS (22). Consistent with these findings, EseC-2HA was accumulated in the TBP in E. piscicida, as revealed by immunoblotting ( Fig.…”

Section: Resultsmentioning

confidence: 99%

The Edwardsiella piscicida Type III Translocon Protein EseC Inhibits Biofilm Formation by Sequestering EseE

Liu

et al. 2019

Appl Environ Microbiol

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The type III secretion system (T3SS) is one of the most important virulence factors of the fish pathogen Edwardsiella piscicida. It contains three translocon proteins, EseB, EseC, and EseD, required for translocation of effector proteins into host cells. We have previously shown that EseB forms filamentous appendages on the surface of E. piscicida, and these filamentous structures mediate bacterial cell-cell interactions promoting autoaggregation and biofilm formation. In the present study, we show that EseC, but not EseD, inhibits the autoaggregation and biofilm formation of E. piscicida. At 18 h postsubculture, a ΔeseC strain developed strong autoaggregation and mature biofilm formation, accompanied by enhanced formation of EseB filamentous appendages. This is in contrast to the weak autoaggregation and immature biofilm formation seen in the E. piscicida wild-type strain. EseE, a protein that directly binds to EseC and also positively regulates the transcription of the escC-eseE operon, was liberated and showed increased levels in the absence of EseC. This led to augmented transcription of the escC-eseE operon, thereby increasing the steady-state protein levels of intracellular EseB, EseD, and EseE, as well as biofilm formation. Notably, the levels of intracellular EseB and EseD produced by the ΔeseE and ΔeseC ΔeseE strains were similar but remarkably lower than those produced by the wild-type strain at 18 h postsubculture. Taken together, we have shown that the translocon protein EseC inhibits biofilm formation through sequestering EseE, a positive regulator of the escC-eseE operon. IMPORTANCE Edwardsiella piscicida, previously known as Edwardsiella tarda, is a Gram-negative intracellular pathogen that mainly infects fish. The type III secretion system (T3SS) plays a pivotal role in its pathogenesis. The T3SS translocon protein EseB is required for the assembly of filamentous appendages on the surface of E. piscicida. The interactions between the appendages facilitate autoaggregation and biofilm formation. In this study, we explored the role of the other two translocon proteins, EseC and EseD, in biofilm formation. We have demonstrated that EseC, but not EseD, inhibits the autoaggregation and biofilm formation of E. piscicida, providing new insights into the regulatory mechanism involved in E. piscicida biofilm formation.

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Functional dissection of translocon proteins of the Salmonella Pathogenicity Island 2-encoded type III secretion system

Cited by 16 publications

References 32 publications

Identification and Functional Characterization of the Novel Edwardsiella tarda Effector EseJ

Identification and Functional Characterization of the Novel Edwardsiella tarda Effector EseJ

Menstrual blood-derived stromal cells modulate functional properties of mouse and human macrophages

The Edwardsiella piscicida Type III Translocon Protein EseC Inhibits Biofilm Formation by Sequestering EseE

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