Abstract
Impaired innate and adaptive immune responses are evidenced throughout the course of PRRSV infection. We previously reported that interleukin-1 receptor antagonist (IL-1Ra) was involved in PRRSV-induced immunosuppression during an early phase of infection. However, the exact mechanism associated with PRRSV-induced IL-1Ra immunomodulation remains unknown. To explore the immunomodulatory properties of PRRSV-induced IL-1Ra on porcine immune functions, monocyte-derived dendritic cells (MoDC) and leukocytes were cultured with type 2 PRRSV, and the immunological role of IL-1Ra was assessed by addition of anti-porcine IL-1Ra Ab. The results demonstrated that PRRSV-induced IL-1Ra reduced phagocytosis, surface expression of MHC II (SLA-DR) and CD86, as well as downregulation of IFNA and IL1 gene expression in the MoDC culture system. Interestingly, IL-1Ra secreted by the PRRSV-infected MoDC also inhibited T lymphocyte differentiation and proliferation, but not IFN-γ production. Although PRRSV-induced IL-1Ra was not directly linked to IL-10 production, it contributed to the differentiation of regulatory T lymphocytes (Treg) within the culture system. Taken together, our results demonstrated that PRRSV-induced IL-1Ra downregulates innate immune functions, T lymphocyte differentiation and proliferation, and influences collectively with IL-10 in the Treg induction. The immunomodulatory roles of IL-1Ra elucidated in this study increase our understanding of the immunobiology of PRRSV.
Highlights
Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) is one of the major pathogens affecting the pig production industry worldwide
To investigate the role of PRRSV-induced interleukin-1 receptor antagonist (IL-1Ra) on porcine innate immune functions, monocyte-derived dendritic cells (MoDC) were infected with type 2 PRRSV or mock (MARC-145 cell lysate) and subsequently
Not to the level of uninfected peripheral blood mononuclear cells (PBMC) (Figure 6B and Supplementary Figure 6B). These findings indicated that PRRSV-induced IL-1Ra might not be directly involved in the development of IL-10-producing T lymphocytes, but could partly play a role in Treg induction under our studied conditions
Summary
Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) is one of the major pathogens affecting the pig production industry worldwide. During an early phase of PRRSV infection, production of type I IFN and pro-inflammatory cytokines (IL-1, IL-6, and TNF-α) was drastically suppressed, leading to uncontrolled viral replication [16, 17]. It has been suggested that PRRSV-induced suppression of innate immunity potentially causes poor adaptive immune responses [18], characterized by attenuated T lymphocyte proliferation, and poor induction of PRRSV-specific IFN-γ-producing cells [19, 20] together with delayed neutralizing antibody responses [21]. Human immunodeficiency virus (HIV)induced IL-1Ra production weakens inflammatory processes through inhibition of IL-1 synthesis in human monocytes [32]. These evidences strongly indicate that IL-1Ra represents a key immunomodulator during an early phase of immune responses. The impact of PRRSV-induced IL-1Ra on porcine innate and adaptive immune functions were investigated
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