PMID- 37099541 OWN - NLM STAT- MEDLINE DCOM- 20230428 LR - 20230511 IS - 1932-6203 (Electronic) IS - 1932-6203 (Linking) VI - 18 IP - 4 DP - 2023 TI - Differential innate immune response of endometrial cells to porcine reproductive and respiratory syndrome virus type 1 versus type 2. PG - e0284658 LID - 10.1371/journal.pone.0284658 [doi] LID - e0284658 AB - 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)-1beta, IL-6 and tumor necrotic factor (TNF)-alpha 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-alpha secretion. In addition, IL-1beta 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. CI - Copyright: (c) 2023 Lothong et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. FAU - Lothong, Muttarin AU - Lothong M AD - Faculty of Veterinary Science, Department of Physiology, Chulalongkorn University, Pathum Wan, Bangkok, Thailand. FAU - Rukarcheep, Dran AU - Rukarcheep D AD - Faculty of Veterinary Science, Department of Physiology, Chulalongkorn University, Pathum Wan, Bangkok, Thailand. FAU - Wattanaphansak, Suphot AU - Wattanaphansak S AD - Faculty of Veterinary Science, Department of Veterinary Medicine, Chulalongkorn University, Pathum Wan, Bangkok, Thailand. FAU - Thammacharoen, Sumpun AU - Thammacharoen S AD - Faculty of Veterinary Science, Department of Physiology, Chulalongkorn University, Pathum Wan, Bangkok, Thailand. FAU - Deachapunya, Chatsri AU - Deachapunya C AD - Faculty of Medicine, Department of Physiology, Srinakharinwirot University, Wattana, Bangkok, Thailand. FAU - Poonyachoti, Sutthasinee AU - Poonyachoti S AUID- ORCID: 0000-0003-3267-8599 AD - Faculty of Veterinary Science, Department of Physiology, Chulalongkorn University, Pathum Wan, Bangkok, Thailand. LA - eng SI - figshare/10.6084/m9.figshare.22303558.v1 SI - figshare/10.6084/m9.figshare.22303543.v2 SI - figshare/10.6084/m9.figshare.22308451.v4 PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20230426 PL - United States TA - PLoS One JT - PloS one JID - 101285081 RN - 0 (Interleukin-6) RN - 0 (Cytokines) RN - 0 (Tumor Necrosis Factor-alpha) RN - 0 (RNA, Messenger) SB - IM MH - Swine MH - Female MH - Animals MH - *Porcine respiratory and reproductive syndrome virus/metabolism MH - *Porcine Reproductive and Respiratory Syndrome MH - Interleukin-6 MH - Immunity, Innate MH - Cytokines/metabolism MH - Tumor Necrosis Factor-alpha MH - Endometrium/metabolism MH - RNA, Messenger/genetics/metabolism PMC - PMC10132667 COIS- The authors have declared that no competing interests exist. EDAT- 2023/04/26 18:42 MHDA- 2023/04/28 06:41 PMCR- 2023/04/26 CRDT- 2023/04/26 13:43 PHST- 2022/11/30 00:00 [received] PHST- 2023/04/04 00:00 [accepted] PHST- 2023/04/28 06:41 [medline] PHST- 2023/04/26 18:42 [pubmed] PHST- 2023/04/26 13:43 [entrez] PHST- 2023/04/26 00:00 [pmc-release] AID - PONE-D-22-31801 [pii] AID - 10.1371/journal.pone.0284658 [doi] PST - epublish SO - PLoS One. 2023 Apr 26;18(4):e0284658. doi: 10.1371/journal.pone.0284658. eCollection 2023.