Transcriptional Profiling of Host Cell Responses to Virulent Haemophilus parasuis: New Insights into Pathogenesis

Abstract

Haemophilus parasuis is the causative agent of Glässer’s disease in pigs. H. parasuis can cause vascular damage, although the mechanism remains unclear. In this study, we investigated the host cell responses involved in the molecular pathway interactions in porcine aortic vascular endothelial cells (PAVECs) induced by H. parasuis using RNA-Seq. The transcriptome results showed that when PAVECs were infected with H. parasuis for 24 h, 281 differentially expressed genes (DEGs) were identified; of which, 236 were upregulated and 45 downregulated. The 281 DEGs were involved in 136 KEGG signaling pathways that were organismal systems, environmental information processing, metabolism, cellular processes, and genetic information processing. The main pathways were the Rap1, FoxO, and PI3K/Akt signaling pathways, and the overexpressed genes were determined and verified by quantitative reverse transcription polymerase chain reaction. In addition, 252 genes were clustered into biological processes, molecular processes, and cellular components. Our study provides new insights for understanding the interaction between bacterial and host cells, and analyzed, in detail, the possible mechanisms that lead to vascular damage induced by H. parasuis. This may lead to development of novel therapeutic targets to control H. parasuis infection.

Chancen und Risiken der Nutzung genetischer Resistenzen gegen Infektionskrankheiten beim Schwein – eine Übersicht

“…Weitere Expressions- und Transkriptomstudien zeigen darüber hinaus, dass bei beiden Erkrankungen die Gene und Stoffwechselwege, welche für die A.-pleuropneumoniae -Resistenz als wesentlich identifiziert wurden, bei der Pathogenese eine Rolle spielen 171 , 172 , 173 , wobei die als zentral identifizierten Stoffwechselwege, basierend auf bisher publizierten Studien, voneinander abweichen. Fu et al 174 identifizierten für die Regulation der Reaktion auf einen Kontakt mit G. parasuis Rap1, FoxO, und PI3K/Akt als hauptsächlich beteiligte Stoffwechselwege. Hierbei muss jedoch berücksichtigt werden, dass in dieser Studie nicht der Gesamtorganismus, sondern die Reaktion isolierter vaskulärer Endothelzellen untersucht wurde.…”

EspP2 Regulates the Adhesion of Glaesserella parasuis via Rap1 Signaling Pathway

“…For instance, Rap1 is required for intracellular bacterial pathogens to form their replication-permissive vacuole [21]. The Rap1 signaling pathway is significantly activated in G. parasuis-infected porcine aortic vascular endothelial cells [22]. The activation of NF-κB in intestinal epithelial cells induced by heat-labile enterotoxins is dependent on the activation of the Ras-like GTPase Rap1 in a cAMP-dependent manner, which in turn promotes the adherence of enterotoxigenic E. coli [23].…”

Transcriptome profiling identifies immune response genes against porcine reproductive and respiratory syndrome virus andHaemophilus parasuisco-infection in the lungs of piglets

“…PRRSV and HPS are resulting in combined infections that exacerbate clinical disease [ 8 ]. Single infections with PRRSV or HPS have been studied by comparison of viral or bacterial loads [ 9 ], pathogenesis [ 10 11 ], clinical syndromes [ 12 ], cytokine production [ 13 ], and transcriptome analysis [ 14 15 ] in pigs or cells. Simultaneous infection with PRRSV and HPS increases inflammatory and immune responses and reduces the production of reactive oxygen species (ROS), which increases the chance of pathogens surviving the host immune response [ 16 17 ].…”