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Differential innate immune response of endometrial cells to porcine reproductive and respiratory syndrome virus type 1 versus type 2. | LitMetric

AI Article Synopsis

  • PRRSV infection in swine leads to significant changes in lung and reproductive system immune responses, which are linked to disease progression, including impacts on pregnancies such as stillbirths and persistent infections.* -
  • The study observed that both PRRSV type 1 and type 2 infections caused noticeable cellular and immune changes in porcine endometrial cells, with type 2 showing more severe effects, such as higher cell infectivity and upregulation of specific immune mediator proteins.* -
  • Key immune responses were altered, with different Toll-like receptors (TLRs) and cytokine expressions being upregulated or downregulated depending on the type of PRRSV, highlighting the complex interactions between the virus and host immune responses

Article Abstract

Modification of cellular and immunological events due to porcine reproductive and respiratory syndrome virus (PRRSV) infection is associated with pathogenesis in lungs. PRRSV also causes female reproductive dysfunction and persistent infection which can spread to fetus, stillbirth, and offspring. In this study, changes in cellular and innate immune responses to PRRSV type 1 or type 2 infection, including expression of PRRSV mediators, mRNA expression of Toll-like receptors (TLRs) and cytokine, and cytokine secretion, were examined in primary porcine glandular endometrial cells (PGE). Cell infectivity as observed by cytopathic effect (CPE), PRRSV nucleocapsid proteins, and viral nucleic acids was detected as early as two days post-infection (2 dpi) and persisted until 6 dpi. A higher percentage of CPE and PRRSV-positive cells were observed in type 2 infections. PRRSV mediator proteins, CD151, CD163, sialoadhesin (Sn), integrin and vimentin, were upregulated following type 1 and type 2 infection. CD151, CD163 and Sn were upregulated by type 2. In both PRRSV types, mRNA expression of TLR1 and TLR6 was upregulated. However, TLR3 was upregulated by type 1, but TLR4 and TLR8 mRNA and protein were downregulated by type 2 only. Interleukin (IL)-1β, IL-6 and tumor necrotic factor (TNF)-α were upregulated by type 2, but IL-8 was upregulated by type 1. Both PRRSV type 1 and 2 stimulated IL-6 but suppressed TNF-α secretion. In addition, IL-1β secretion was suppressed only by type 2. These findings reveal an important mechanism underlying the strategy of PRRSV infection in the endometrium and associated with the viral persistence.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10132667PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0284658PLOS

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