Limits...
SPI-1-encoded type III secretion system of Salmonella enterica is required for the suppression of porcine alveolar macrophage cytokine expression.

Pavlova B, Volf J, Ondrackova P, Matiasovic J, Stepanova H, Crhanova M, Karasova D, Faldyna M, Rychlik I - Vet. Res. (2011)

Bottom Line: Typhimurium and S.The hilA mutant exhibited an intermediate phenotype between the ΔSPI1 mutant and the wild-type S.Enteritidis.

View Article: PubMed Central - HTML - PubMed

Affiliation: Veterinary Research Institute, Brno, Czech Republic. rychlik@vri.cz.

ABSTRACT
Genes localized at Salmonella pathogenicity island-1 (SPI-1) are involved in Salmonella enterica invasion of host non-professional phagocytes. Interestingly, in macrophages, SPI-1-encoded proteins, in addition to invasion, induce cell death via activation of caspase-1 which also cleaves proIL-1β and proIL-18, precursors of 2 proinflammatory cytokines. In this study we were therefore interested in whether SPI-1-encoded type III secretion system (T3SS) may influence proinflammatory response of macrophages. To test this hypothesis, we infected primary porcine alveolar macrophages with wild-type S. Typhimurium and S. Enteritidis and their isogenic SPI-1 deletion mutants. ΔSPI1 mutants of both serovars invaded approx. 5 times less efficiently than the wild-type strains and despite this, macrophages responded to the infection with ΔSPI1 mutants by increased expression of proinflammatory cytokines IL-1β, IL-8, TNFα, IL-23α and GM-CSF. Identical macrophage responses to that induced by the ΔSPI1 mutants were also observed to the infection with sipB but not the sipA mutant. The hilA mutant exhibited an intermediate phenotype between the ΔSPI1 mutant and the wild-type S. Enteritidis. 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.

Show MeSH

Related in: MedlinePlus

Cytokine expression of PAMs infected with the wild-type S. Enteritidis, sipA, hilA, ΔSPI1 and sipB mutants, and non-infected cells (n.i.).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3037896&req=5

Figure 3: Cytokine expression of PAMs infected with the wild-type S. Enteritidis, sipA, hilA, ΔSPI1 and sipB mutants, and non-infected cells (n.i.).

Mentions: Since Boyen et al. reported that a hilA mutant of S. Typhimurium stimulated the production of IL-8 by PAMs similarly as did the wild-type strain [15], i.e. different from our observations with the ΔSPI1 mutant, and because Murray and Lee reported on different behavior of ΔSPI1 and hilA mutants in mice [2], we tested the cytokine response of PAMs to hilA, sipB and sipA mutants of S. Enteritidis in the final experiment. For this experiment we only selected 6 cytokines which responded the most in the previous experiments to Salmonella infection. The fully invasive sipA mutant never differed in stimulation of the cytokine response from the wild-type S. Enteritidis. hilA and sipB mutants were of reduced invasiveness (Figure 1) and 4 h after the infection, these mutants stimulated cytokine expression of PAMs similar to the ΔSPI1 mutant i.e. higher than did the wild-type S. Enteritidis. Interestingly, 24 h post infection, while the sipB mutant still behaved similarly to the ΔSPI1 mutant, the hilA mutant no longer stimulated the expression of IL-1β, IL-8, IL-12β or IL-23α more than did the wild-type S. Enteritidis (Figure 3).


SPI-1-encoded type III secretion system of Salmonella enterica is required for the suppression of porcine alveolar macrophage cytokine expression.

Pavlova B, Volf J, Ondrackova P, Matiasovic J, Stepanova H, Crhanova M, Karasova D, Faldyna M, Rychlik I - Vet. Res. (2011)

Cytokine expression of PAMs infected with the wild-type S. Enteritidis, sipA, hilA, ΔSPI1 and sipB mutants, and non-infected cells (n.i.).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3037896&req=5

Figure 3: Cytokine expression of PAMs infected with the wild-type S. Enteritidis, sipA, hilA, ΔSPI1 and sipB mutants, and non-infected cells (n.i.).
Mentions: Since Boyen et al. reported that a hilA mutant of S. Typhimurium stimulated the production of IL-8 by PAMs similarly as did the wild-type strain [15], i.e. different from our observations with the ΔSPI1 mutant, and because Murray and Lee reported on different behavior of ΔSPI1 and hilA mutants in mice [2], we tested the cytokine response of PAMs to hilA, sipB and sipA mutants of S. Enteritidis in the final experiment. For this experiment we only selected 6 cytokines which responded the most in the previous experiments to Salmonella infection. The fully invasive sipA mutant never differed in stimulation of the cytokine response from the wild-type S. Enteritidis. hilA and sipB mutants were of reduced invasiveness (Figure 1) and 4 h after the infection, these mutants stimulated cytokine expression of PAMs similar to the ΔSPI1 mutant i.e. higher than did the wild-type S. Enteritidis. Interestingly, 24 h post infection, while the sipB mutant still behaved similarly to the ΔSPI1 mutant, the hilA mutant no longer stimulated the expression of IL-1β, IL-8, IL-12β or IL-23α more than did the wild-type S. Enteritidis (Figure 3).

Bottom Line: Typhimurium and S.The hilA mutant exhibited an intermediate phenotype between the ΔSPI1 mutant and the wild-type S.Enteritidis.

View Article: PubMed Central - HTML - PubMed

Affiliation: Veterinary Research Institute, Brno, Czech Republic. rychlik@vri.cz.

ABSTRACT
Genes localized at Salmonella pathogenicity island-1 (SPI-1) are involved in Salmonella enterica invasion of host non-professional phagocytes. Interestingly, in macrophages, SPI-1-encoded proteins, in addition to invasion, induce cell death via activation of caspase-1 which also cleaves proIL-1β and proIL-18, precursors of 2 proinflammatory cytokines. In this study we were therefore interested in whether SPI-1-encoded type III secretion system (T3SS) may influence proinflammatory response of macrophages. To test this hypothesis, we infected primary porcine alveolar macrophages with wild-type S. Typhimurium and S. Enteritidis and their isogenic SPI-1 deletion mutants. ΔSPI1 mutants of both serovars invaded approx. 5 times less efficiently than the wild-type strains and despite this, macrophages responded to the infection with ΔSPI1 mutants by increased expression of proinflammatory cytokines IL-1β, IL-8, TNFα, IL-23α and GM-CSF. Identical macrophage responses to that induced by the ΔSPI1 mutants were also observed to the infection with sipB but not the sipA mutant. The hilA mutant exhibited an intermediate phenotype between the ΔSPI1 mutant and the wild-type S. Enteritidis. 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.

Show MeSH
Related in: MedlinePlus