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

PLoS One. 2023 Apr 26;18(4):e0284658. doi: 10.1371/journal.pone.0284658. eCollection 2023.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cytokines / metabolism
  • Endometrium / metabolism
  • Female
  • Immunity, Innate
  • Interleukin-6
  • Porcine Reproductive and Respiratory Syndrome*
  • Porcine respiratory and reproductive syndrome virus* / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Swine
  • Tumor Necrosis Factor-alpha


  • Interleukin-6
  • Cytokines
  • Tumor Necrosis Factor-alpha
  • RNA, Messenger

Associated data

  • figshare/10.6084/m9.figshare.22303558.v1
  • figshare/10.6084/m9.figshare.22303543.v2
  • figshare/10.6084/m9.figshare.22308451.v4

Grants and funding

SP was funded by CU-56-644-HR, CU_FRB640001_01_31_4 and GRB_BSS_73_58_31_04 Ratchadapiseksomphot Endowment Fund and Chulalongkorn University (https://www.research.chula.ac.th/). ML was funded by GCUGR1125604041D/2560 the 90th and 100th Anniversary of Chulalongkorn University Fund. CD was funded by 135/2558 Srinakharinwirot University. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.