Muramylpeptide shedding modulates cell sensing of Shigella flexneri

Nigro, Giulia; Fazio, Luigi Lembo; Martino, Maria Celeste; Rossi, Giacomo; Tattoli, Ivan; Liparoti, Valeria; Castro, Cristina De; Molinaro, Antonio; Philpott, Dana J.; Bernardini, Maria Lina

doi:10.1111/j.1462-5822.2007.01075.x

Cited by 67 publications

(82 citation statements)

References 52 publications

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“…S3A) and PGN ( Fig. S3 B and C) in HEK 293 cells expressing TLR2 (i.e., BLPs) or hNod1 or hNod2 (i.e., PGN) (34). Then, LPSs were assessed in bone marrow-derived macrophages (BMDMs) in the presence or absence of Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (OxPAPC)C (40 μg/mL; Fig.…”

Section: Activation Of Nf-κb By Lps Extracted From Acellular and Intrmentioning

confidence: 99%

IntracellularShigellaremodels its LPS to dampen the innate immune recognition and evade inflammasome activation

Paciello¹,

Silipo

Fazio³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Section: Activation Of Nf-κb By Lps Extracted From Acellular and Intrmentioning

confidence: 99%

IntracellularShigellaremodels its LPS to dampen the innate immune recognition and evade inflammasome activation

Paciello¹,

Silipo

Fazio³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…One possible explanation is that the Pdi-dependent ability of S. iniae to form longer chains reduces the efficiency of phagocytic uptake and clearance. Another possible explanation for this decreased survival is that deacetylation of S. iniae cell surface molecules introduces significant changes in molecular patterns that are otherwise easily recognized by the host immune system, thus allowing WT S. iniae to survive and persist in vivo (Arancibia et al, 2007;Nigro et al, 2008). In examining specific potential effectors of phagocytic killing, we have found no difference in the kinetics of the killing of WT and Dpdi by hydrogen peroxide (a component of the oxidative burst) and the cationic HSB AMP moronecidin.…”

Section: Discussionmentioning

confidence: 99%

The novel polysaccharide deacetylase homologue Pdi contributes to virulence of the aquatic pathogen Streptococcus iniae

et al. 2010

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The aquatic zoonotic pathogen Streptococcus iniae represents a threat to the worldwide aquaculture industry and poses a risk to humans who handle raw fish. Because little is known about the mechanisms of S. iniae pathogenesis or virulence factors, we established a highthroughput system combining whole-genome pyrosequencing and transposon mutagenesis that allowed us to identify virulence proteins, including Pdi, the polysaccharide deacetylase of S. iniae, that we describe here. Using bioinformatics tools, we identified a highly conserved signature motif in Pdi that is also conserved in the peptidoglycan deacetylase PgdA protein family. A Dpdi mutant was attenuated for virulence in the hybrid striped bass model and for survival in whole fish blood. Moreover, Pdi was found to promote bacterial resistance to lysozyme killing and the ability to adhere to and invade epithelial cells. On the other hand, there was no difference in the autolytic potential, resistance to oxidative killing or resistance to cationic antimicrobial peptides between S. iniae wild-type and Dpdi. In conclusion, we have demonstrated that pdi is involved in S. iniae adherence and invasion, lysozyme resistance and survival in fish blood, and have shown that pdi plays a role in the pathogenesis of S. iniae. Identification of Pdi and other S. iniae virulence proteins is a necessary initial step towards the development of appropriate preventive and therapeutic measures against diseases and economic losses caused by this pathogen. INTRODUCTIONIn the past few decades, the pathogen Streptococcus iniae has emerged as a major hindrance to aquaculture operations worldwide (Agnew & Barnes, 2007), causing economic losses measured in hundreds of millions of dollars annually. In addition, S. iniae has established itself as a zoonotic risk, especially in areas of the world that preferentially prepare and consume raw fish (Lau et al., 2003). To date, at least 25 human cases of invasive streptococcal infection attributed to S. iniae have been confirmed in the USA, Canada, China and Taiwan, many of which were in immunocompromised patients (Agnew & Barnes, 2007;Sun et al., 2007;Weinstein et al., 1997); since there is currently no prospective epidemiological surveillance for human S. iniae infections, the true number may be much higher (Facklam et al., 2005;Lau et al., 2006).In spite of the economic and human health risks that S. iniae presents, a fully assembled genome sequence for this emerging pathogen is not yet available, and very little is known about its disease mechanisms. To better understand the molecular genetic basis of virulence in this versatile pathogen, we created a library of randomly generated transposon mutants that we screened for virulence Abbreviations: AMP, antimicrobial peptide; HSB, hybrid striped bass, i.p., intraperitoneal; PIA, polysaccharide intercellular adhesin, WT, wild-type.3These authors contributed equally to this work.The GenBank/EMBL/DDBJ accession number for the pdi sequence of Streptococcus iniae is FJ664396.Four supplementary f...

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“…3A). Indeed, it was shown that muramylpeptides shed by Shigella in epithelial cells are able to trigger Nod1-mediated NF-kB activation [18]. Muramylpeptides can be also generated in the cytosol after invasion by Gram-positive bacteria.…”

Section: Nod2-dependent Nf-kb and Mapks Activation Pathways In Responmentioning

confidence: 99%

The protein Nod2: An innate receptor more complex than previously assumed

Lecat

Piette

Legrand-Poels

2010

Biochemical Pharmacology

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Please check your proof carefully and mark all corrections at the appropriate place in the proof (e.g., by using on-screen annotation in the PDF file) or compile them in a separate list.For correction or revision of any artwork, please consult http://www.elsevier.com/artworkinstructions.Any queries or remarks that have arisen during the processing of your manuscript are listed below and highlighted by flags in the proof. Click on the 'Q' link to go to the location in the proof. Location inQuery / Remark: click on the Q link to go article Please insert your reply or correction at the corresponding line in the proof Q1If there are fewer than seven authors, please supply all their names; if there are seven or more authors, please supply the first six authors' names, followed by 'et al.'Thank you for your assistance. Graphical AbstractBiochemical Pharmacology xxx (2010) xxx-xxx pp: xxx-xxx The protein Nod2: An innate receptor more complex than previously assumed

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Muramylpeptide shedding modulates cell sensing of Shigella flexneri

Cited by 67 publications

References 52 publications

IntracellularShigellaremodels its LPS to dampen the innate immune recognition and evade inflammasome activation

IntracellularShigellaremodels its LPS to dampen the innate immune recognition and evade inflammasome activation

The novel polysaccharide deacetylase homologue Pdi contributes to virulence of the aquatic pathogen Streptococcus iniae

The protein Nod2: An innate receptor more complex than previously assumed

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