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

• Main Authors: Pavlova Barbora, Volf Jiri, Ondrackova Petra, Matiasovic Jan, Stepanova Hana, Crhanova Magdalena, Karasova Daniela, Faldyna Martin, Rychlik Ivan
• Format: Article
• Language: English
• Published: BMC 2011-01-01
• Series: Veterinary Research
• Online Access: http://www.veterinaryresearch.org/content/42/1/16

<p>Abstract</p> <p>Genes localized at <it>Salmonella </it>pathogenicity island-1 (SPI-1) are involved in <it>Salmonella enterica </it>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 <it>S</it>. Typhimurium and <it>S</it>. 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 <it>sipB </it>but not the <it>sipA </it>mutant. The <it>hilA </it>mutant exhibited an intermediate phenotype between the ΔSPI1 mutant and the wild-type <it>S</it>. 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.</p>