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Statements

Subject Item
n2:RIV%2F00027162%3A_____%2F11%3A%230000751%21RIV12-MZE-00027162
rdf:type
skos:Concept n11:Vysledek
dcterms:description
Genes localized at Salmonella pathogenicity island-1 (SPI-1) are involved in Salmonella invasion of host non-professional phagocytes. In addition to invasion, SPI-1-encoded proteins induce cell death of macrophages via activation of caspase-1 which also cleaves proIL-1 beta and proIL-18, precursors of 2 proinflammatory cytokines. We were therefore interested in whether SPI-1-encoded type III secretion system (T3SS) may influence proinflammatory response of macrophages. We infected primary porcine alveolar macrophages with wild-type S. Typhimurium and S. Enteritidis and their SPI-1 deletion mutants. SPI1 mutants of both serovars invaded approx. 5 times less efficiently than the wild-type strains and despite this, macrophages responded to the infection with Delta SPI1 mutants by increased expression of proinflammatory cytokines. Our results showed that the SPI-1-encoded T3SS is required not only for cell invasion but in macrophages also for the suppression of early proinflammatory cytokine expression. Genes localized at Salmonella pathogenicity island-1 (SPI-1) are involved in Salmonella invasion of host non-professional phagocytes. In addition to invasion, SPI-1-encoded proteins induce cell death of macrophages via activation of caspase-1 which also cleaves proIL-1 beta and proIL-18, precursors of 2 proinflammatory cytokines. We were therefore interested in whether SPI-1-encoded type III secretion system (T3SS) may influence proinflammatory response of macrophages. We infected primary porcine alveolar macrophages with wild-type S. Typhimurium and S. Enteritidis and their SPI-1 deletion mutants. SPI1 mutants of both serovars invaded approx. 5 times less efficiently than the wild-type strains and despite this, macrophages responded to the infection with Delta SPI1 mutants by increased expression of proinflammatory cytokines. Our results showed that the SPI-1-encoded T3SS is required not only for cell invasion but in macrophages also for the suppression of early proinflammatory cytokine expression.
dcterms:title
SPI-1-encoded type III secretion system of Salmonella enterica is required for the suppression of porcine alveolar macrophage cytokine expression SPI-1-encoded type III secretion system of Salmonella enterica is required for the suppression of porcine alveolar macrophage cytokine expression
skos:prefLabel
SPI-1-encoded type III secretion system of Salmonella enterica is required for the suppression of porcine alveolar macrophage cytokine expression SPI-1-encoded type III secretion system of Salmonella enterica is required for the suppression of porcine alveolar macrophage cytokine expression
skos:notation
RIV/00027162:_____/11:#0000751!RIV12-MZE-00027162
n11:predkladatel
n12:ico%3A00027162
n3:aktivita
n16:P n16:Z
n3:aktivity
P(1B44020), P(ED0006/01/01), P(GA524/08/1606), Z(MZE0002716202)
n3:cisloPeriodika
16
n3:dodaniDat
n8:2012
n3:domaciTvurceVysledku
n7:7331614 n7:2888955 n7:9231625 n7:7153643 n7:9736948 n7:3656446 n7:7872275 n7:5548721 n7:7362366
n3:druhVysledku
n18:J
n3:duvernostUdaju
n19:S
n3:entitaPredkladatele
n20:predkladatel
n3:idSjednocenehoVysledku
231474
n3:idVysledku
RIV/00027162:_____/11:#0000751
n3:jazykVysledku
n9:eng
n3:klicovaSlova
NITRIC-OXIDE PRODUCTION; SEROVAR TYPHIMURIUM; PATHOGENICITY ISLANDS; SPI-1 GENES; CELL-DEATH; APOPTOSIS; INVASION; SIPB; ENTERITIDIS; CASPASE-1
n3:klicoveSlovo
n5:PATHOGENICITY%20ISLANDS n5:ENTERITIDIS n5:CASPASE-1 n5:CELL-DEATH n5:NITRIC-OXIDE%20PRODUCTION n5:APOPTOSIS n5:INVASION n5:SPI-1%20GENES n5:SIPB n5:SEROVAR%20TYPHIMURIUM
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[A20432429C61]
n3:nazevZdroje
Veterinary Research
n3:obor
n14:GJ
n3:pocetDomacichTvurcuVysledku
9
n3:pocetTvurcuVysledku
9
n3:projekt
n4:ED0006%2F01%2F01 n4:1B44020 n4:GA524%2F08%2F1606
n3:rokUplatneniVysledku
n8:2011
n3:svazekPeriodika
42
n3:tvurceVysledku
Matiašovic, Ján Štěpánová, Hana Pavlová, Barbora Ondráčková, Petra Volf, Jiří Karasová, Daniela Faldyna, Martin Crhánová, Magdaléna Rychlík, Ivan
n3:wos
000290659600005
n3:zamer
n6:MZE0002716202
s:issn
0928-4249
s:numberOfPages
6
n10:doi
10.1186/1297-9716-42-16