Centre de Recerca en Sanitat Animal (CReSA), UAB-IRTA, Campus de la Universitat Autònoma de Barcelona (UAB), 08193 Bellaterra, Barcelona, Spain.
Vet Res. 2012 Nov 16;43(1):80. doi: 10.1186/1297-9716-43-80.
Pigs possess a microbiota in the upper respiratory tract that includes Haemophilus parasuis. Pigs are also considered the reservoir of influenza viruses and infection with this virus commonly results in increased impact of bacterial infections, including those by H. parasuis. However, the mechanisms involved in host innate responses towards H. parasuis and their implications in a co-infection with influenza virus are unknown. Therefore, the ability of a non-virulent H. parasuis serovar 3 (SW114) and a virulent serovar 5 (Nagasaki) strains to interact with porcine bone marrow dendritic cells (poBMDC) and their modulation in a co-infection with swine influenza virus (SwIV) H3N2 was examined. At 1 hour post infection (hpi), SW114 interaction with poBMDC was higher than that of Nagasaki, while at 8 hpi both strains showed similar levels of interaction. The co-infection with H3N2 SwIV and either SW114 or Nagasaki induced higher levels of IL-1β, TNF-α, IL-6, IL-12 and IL-10 compared to mock or H3N2 SwIV infection alone. Moreover, IL-12 and IFN-α secretion differentially increased in cells co-infected with H3N2 SwIV and Nagasaki. These results pave the way for understanding the differences in the interaction of non-virulent and virulent strains of H. parasuis with the swine immune system and their modulation in a viral co-infection.
猪的上呼吸道存在包括副猪嗜血杆菌(Haemophilus parasuis)在内的微生物群落。猪也被认为是流感病毒的储存宿主,感染这种病毒通常会增加细菌感染的影响,包括副猪嗜血杆菌感染。然而,宿主先天对副猪嗜血杆菌的反应机制及其在与流感病毒共同感染中的影响尚不清楚。因此,本研究检测了非毒性副猪嗜血杆菌血清型 3 株(SW114)和毒性血清型 5 株(Nagasaki)与猪骨髓树突状细胞(poBMDC)相互作用的能力,以及它们在与猪流感病毒(SwIV)H3N2 共同感染时的调节作用。感染后 1 小时(hpi),SW114 与 poBMDC 的相互作用高于 Nagasaki,而在 8 hpi 时,两种菌株的相互作用水平相似。与单独感染 H3N2 SwIV 或 mock 相比,H3N2 SwIV 与 SW114 或 Nagasaki 的共同感染诱导了更高水平的 IL-1β、TNF-α、IL-6、IL-12 和 IL-10。此外,在 H3N2 SwIV 和 Nagasaki 共同感染的细胞中,IL-12 和 IFN-α 的分泌差异增加。这些结果为理解非毒性和毒性副猪嗜血杆菌菌株与猪免疫系统的相互作用差异以及它们在病毒共同感染中的调节作用奠定了基础。