Involvement of NF-kappaB and MAP-kinases in the transcriptional response of alveolar macrophages to Streptococcus suis

Abstract

Interaction of Streptococcus suis with primary porcine alveolar macrophages was studied using transcriptomics. Transcriptional response of macrophages to two different S. suis strains was studied: wild-type S10 that is resistant to phagocytosis, and its non-encapsulated mutant that is phagocytosed efficiently. The macrophages' transcriptional response was observed only after 60 min of incubation. Eleven genes were expressed significantly different between macrophages infected with streptococci and control mock-infected macrophages. These genes include IL-1-beta, MIP-2-alpha and TNF-alpha. When gene expression was studied as a function of time, transcriptional changes occurred in all macrophages independent of streptococci. The fold induction of induced genes however, was much stronger in macrophages incubated with the non-encapsulated S. suis strain that was phagocytosed. The genes that were higher induced due to S. suis suggest an innate immune response is induced in macrophages. Pathway analysis revealed that genes that are part of the putative MAP-kinase signal transduction system are over-represented among the regulated genes. Using an immortalized alveolar macrophage cell line it was shown that macrophages respond to interaction with S. suis by the translocation of NF-kappaB to the nucleus, independent of phagocytosis. This translocation subsequently induced expression of innate immune genes. This strongly suggests besides the MAP-kinase signaling pathway, NF-kappaB signaling is also induced upon interaction with S. suis.