scholarly journals Role of Maturation of Lipoproteins in the Pathogenesis of the Infection Caused by Streptococcus suis Serotype 2

2021 ◽  
Vol 9 (11) ◽  
pp. 2386
Author(s):  
Servane Payen ◽  
David Roy ◽  
Anaïs Boa ◽  
Masatoshi Okura ◽  
Jean-Philippe Auger ◽  
...  
Keyword(s):  
Bacterial Pathogen ◽  
Streptococcus Suis ◽  
Signal Peptidase ◽  
Phagocytic Cells ◽  
Suis Serotype ◽  
Highly Virulent ◽  
Streptococcus Suis Serotype 2

Streptococcus suis serotype 2 is an important porcine bacterial pathogen associated with multiple pathologies in piglets. Bacterial lipoproteins (LPPs) have been described as playing important roles in the pathogenesis of the infection of other Gram-positive bacteria as adhesins, pro-inflammatory cell activators and/or virulence factors. In the current study, we aimed to evaluate the role of the prolipoprotein diacylglyceryl transferase (Lgt) and lipoprotein signal peptidase (Lsp) enzymes, which are responsible for LPP maturation, on the pathogenesis of the infection caused by two different sequence types (STs) of S. suis serotype 2 strains (virulent ST1 and highly virulent ST7). Through the use of isogenic Δlgt, Δlsp and double Δlgt/Δlsp mutants, it was shown that lack of these enzymes did not influence S. suis adhesion/invasion to porcine respiratory epithelial cells. However, in the absence of the Lsp and/or Lgt, a significant reduction in the capacity of S. suis to activate phagocytic cells and induce pro-inflammatory mediators (in vitro and in vivo) was observed. In general, results obtained with the double mutant did not differ in comparison to single mutants, indicating lack of an additive effect. Finally, our data suggest that these enzymes play a differential role in virulence, depending on the genetic background of the strain and being more important for the highly virulent ST7 strain.

scholarly journals Recognition of Lipoproteins by Toll-like Receptor 2 and DNA by the AIM2 Inflammasome Is Responsible for Production of Interleukin-1β by Virulent Suilysin-Negative Streptococcus suis Serotype 2

Pathogens ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 147 ◽  
Author(s):  
Agustina Lavagna ◽  
Jean-Philippe Auger ◽  
Stephen E. Giradin ◽  
Nicolas Gisch ◽  
Mariela Segura ◽  
...  
Keyword(s):  
Bacterial Pathogen ◽  
Systemic Infection ◽  
Streptococcus Suis ◽  
Bacterial Burden ◽  
Toll Like Receptor ◽  
Internalization Rate ◽  
Toll Like Receptor 2 ◽  
Suis Serotype ◽  
Streptococcus Suis Serotype 2

Streptococcus suis serotype 2 is an important porcine bacterial pathogen and zoonotic agent causing sudden death, septic shock and meningitis. These pathologies are the consequence of an exacerbated inflammatory response composed of various mediators including interleukin (IL)-1β. Elevated levels of the toxin suilysin (SLY) were demonstrated to play a key role in S. suis-induced IL-1β production. However, 95% of serotype 2 strains isolated from diseased pigs in North America, many of which are virulent, do not produce SLY. In this study, we demonstrated that SLY-negative S. suis induces elevated levels of IL-1β in systemic organs, with dendritic cells contributing to this production. SLY-negative S. suis-induced IL-1β production requires MyD88 and TLR2 following recognition of lipoproteins. However, the higher internalization rate of the SLY-negative strain results in intracellularly located DNA being recognized by the AIM2 inflammasome, which promotes IL-1β production. Finally, the role of IL-1 in host survival during the S. suis systemic infection is beneficial and conserved, regardless of SLY production, via modulation of the inflammation required to control bacterial burden. In conclusion, this study demonstrates that SLY is not required for S. suis-induced IL-1β production.

Lipoprotein signal peptidase of Streptococcus suis serotype 2

Microbiology ◽  
2003 ◽  
Vol 149 (6) ◽  
pp. 1399-1407 ◽  
Author(s):  
Astrid de Greeff ◽  
Andrea Hamilton ◽  
Iain C. Sutcliffe ◽  
Herma Buys ◽  
Loek van Alphen ◽  
...  
Keyword(s):  
Wild Type Strain ◽  
Streptococcus Suis ◽  
Signal Peptidase ◽  
Wild Type ◽  
Knockout Mutant ◽  
E Coli ◽  
Translation Systems ◽  
Suis Serotype

This paper reports the complete coding sequence for a proliprotein signal peptidase (SP-ase) of Streptococcus suis, Lsp. This is believed to be the first SP-ase described for S. suis. SP-ase II is involved in the removal of the signal peptide from glyceride-modified prolipoproteins. By using in vitro transcription/translation systems, it was shown that the lsp gene was transcribed in vitro. Functionality of Lsp in Escherichia coli was demonstrated by using an in vitro globomycin resistance assay, to show that expression of Lsp in E. coli increased the globomycin resistance. An isogenic mutant of S. suis serotype 2 unable to produce Lsp was constructed and shown to process lipoproteins incorrectly, including an S. suis homologue of the pneumococcal PsaA lipoprotein. Five piglets were inoculated with a mixture of both strains in an experimental infection, to determine the virulence of the mutant strain relative to that of the wild-type strain in a competitive challenge experiment. The data showed that both strains were equally virulent, indicating that the knockout mutant of lsp is not attenuated in vivo.

scholarly journals Streptococcus suis Serotype 2 Capsule In Vivo

2016 ◽  
Vol 22 (10) ◽  
pp. 1793-1796 ◽  
Author(s):  
Jean-Philippe Auger ◽  
Nattakan Meekhanon ◽  
Masatoshi Okura ◽  
Makoto Osaki ◽  
Marcelo Gottschalk ◽  
...  
Keyword(s):  
Streptococcus Suis ◽  
Suis Serotype ◽  
Streptococcus Suis Serotype 2

Differential role of MyD88 signaling in Streptococcus suis serotype 2-induced systemic and central nervous system diseases

2019 ◽  
Vol 31 (11) ◽  
pp. 697-714 ◽  
Author(s):  
Jean-Philippe Auger ◽  
Marie-Odile Benoit-Biancamano ◽  
Christian Bédard ◽  
Mariela Segura ◽  
Marcelo Gottschalk
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Streptococcus Suis ◽  
Nervous System Diseases ◽  
Central Nervous System Diseases ◽  
Myd88 Signaling ◽  
Suis Serotype ◽  
Streptococcus Suis Serotype 2

MyD88 signaling modulates the outcome of Streptococcus suis infection

scholarly journals In vitro Transcriptome Analysis of Two Chinese Isolates of Streptococcus suis Serotype 2

2014 ◽  
Vol 12 (6) ◽  
pp. 266-275
Author(s):  
Dake Zhang ◽  
Nan Du ◽  
Sufang Ma ◽  
Qingtao Hu ◽  
Guangwen Lu ◽  
...  
Keyword(s):  
Transcriptome Analysis ◽  
Streptococcus Suis ◽  
Suis Serotype ◽  
Streptococcus Suis Serotype 2

scholarly journals Role of AFR1, an ABC Transporter-Encoding Gene, in the In Vivo Response to Fluconazole and Virulence of Cryptococcus neoformans

2006 ◽  
Vol 74 (2) ◽  
pp. 1352-1359 ◽  
Author(s):  
Maurizio Sanguinetti ◽  
Brunella Posteraro ◽  
Marilena La Sorda ◽  
Riccardo Torelli ◽  
Barbara Fiori ◽  
...  
Keyword(s):  
Cryptococcus Neoformans ◽  
Abc Transporter ◽  
Phagocytic Cells ◽  
Macrophage Infection ◽  
Encoding Gene ◽  
Fungal Tissue ◽  
Intravenous Inoculation

ABSTRACT We have recently demonstrated that upregulation of the ATP binding cassette (ABC) transporter-encoding gene AFR1 in Cryptococcus neoformans is involved in the in vitro resistance to fluconazole of this yeast. In the present study, we investigated the role of AFR1 in the in vivo response to fluconazole in a mouse model of systemic cryptococcosis. Mice were infected with a wild-type fluconazole-susceptible strain of C. neoformans, strain BPY22; an afr1 mutant, BPY444, which displayed hypersusceptibility to fluconazole in vitro; or an AFR1-overexpressing strain, BPY445, which exhibited in vitro resistance to the drug. In each of the three groups, infected animals were randomly assigned to fluconazole treatment or untreated-control subgroups. As expected, fluconazole prolonged survival and reduced fungal tissue burdens (compared with no treatment) in BPY22- and BPY444-infected mice, whereas it had no significant effects in mice infected with BPY445. When the pathogenicities of these strains in mice were investigated, strain BPY445 was significantly more virulent than BPY22 following inhalational or intravenous inoculation, but mice infected with BPY444 survived significantly longer than BPY22-infected animals only when infection was acquired via the respiratory tract. In in vitro macrophage infection studies, strain BPY445 also displayed enhanced intracellular survival compared with strains BPY22 and BPY444, suggesting that its increased virulence may be due to its reduced vulnerability to the antimicrobial factors produced by phagocytic cells. These findings indicate that the upregulation of the AFR1 gene is an important factor in either determining the in vivo resistance to fluconazole or influencing the virulence of C. neoformans.

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