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Porcine Fc?RI Mediates Porcine Reproductive and Respiratory Syndrome Virus Multiplication and Regulates the Inflammatory Reaction.

ABSTRACT: Porcine reproductive and respiratory syndrome virus (PRRSV) shows characteristic antibody-dependent enhancement (ADE) of infection and causes porcine systemic inflammation, which is similar to a type I allergic reaction; however, the role of porcine Fc?RI in ADE is still unclear. In this study, the expression of different Fc receptors (FcRs) on macrophages was investigated in a PRRSV 3D4/21 cell infection model in the presence or absence of PRRSV antibody. The transcription level of Fc?II and Fc?RI was significantly up-regulated under PRRSV-antibody complex infection. Internalization and proliferation of PRRSV were promoted by the ADE mechanism when Fc?RI was expressed in permissive 3D4/21 cells and the non-permissive cell line HEK 293T. Transcriptome sequencing data showed that the expression levels of AKT, ERK and other signal molecules in the anti-inflammatory pathway were significantly increased, especially in the cells infected with the PRRSV-antibody immune complex. Inflammatory regulatory molecules such as PLA2G6, LOX, TRPM8 and TRPM4 were significantly up-regulated following PRRSV infection but significantly down-regulated in the cells infected with the PRRSV-antibody immune complex. Our results demonstrated that Fc?RI could be involved in PRRSV ADE, the antigen presenting process and regulation of the inflammatory response during PRRSV infection, which provides new insights into PRRSV infection mediated by Fc?RI and the PRRSV-antibody immune complex.

SUBMITTER: Shi P

PROVIDER: S-EPMC6178556 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

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Porcine FcεRI Mediates Porcine Reproductive and Respiratory Syndrome Virus Multiplication and Regulates the Inflammatory Reaction.

Shi Peidian P Zhang Lilin L Wang Jiashun J Lu Dong D Li Yi Y Ren Jie J Shen Menglu M Zhang Lei L Huang Jinhai J

Virologica Sinica 20180514 3

Porcine reproductive and respiratory syndrome virus (PRRSV) shows characteristic antibody-dependent enhancement (ADE) of infection and causes porcine systemic inflammation, which is similar to a type I allergic reaction; however, the role of porcine FcεRI in ADE is still unclear. In this study, the expression of different Fc receptors (FcRs) on macrophages was investigated in a PRRSV 3D4/21 cell infection model in the presence or absence of PRRSV antibody. The transcription level of FcγII and Fc ...[more]

PMID: 29761267

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Project description:The objective of this study was to estimate genetic parameters of antibody response and reproductive traits after exposure to porcine reproductive and respiratory syndrome virus. Blood samples were taken approximately 60 d after the outbreak. Antibody levels were quantified as the sample-to-positive ratio (S/P ratio) using a fluorescent microsphere assay. Reproductive traits included total number born (TNB), number born alive (NBA), number stillborn (NSB), number mummified (NBM), and number born dead (NBD). Mortality traits were log transformed for genetic analyses. Data were split into prior, during, and after the disease outbreak phases using visual appraisal of the estimates of farm-year-week effects for each reproductive trait. For NBA, data from all phases were combined into a reaction norm analysis with regression on estimates of farm-year-week effects for NBA. Heritability for S/P ratio was estimated at 0.17 ± 0.05. Heritability estimates for reproduction traits were all low and were lower during the outbreak for NBA but greater for mortality traits. TNB was not greatly affected during the outbreak, as many sows that farrowed during the outbreak were mated prior to the outbreak. Heritability for TNB decreased from 0.13 (prior) to 0.08 (after). Genetic correlation estimates between prior to and during the outbreak were high for TNB (0.86 ± 0.23) and NBA (0.98 ± 0.38) but lower for mortality traits: 0.65 ± 0.43, -0.42 ± 0.55, and 0.29 ± 1.39 for LNSB, LNBM, and LNBD, respectively. TNB prior to and after the outbreak had a lower genetic correlation (0.32 ± 0.33). In general, genetic correlation estimates of S/P ratio with reproductive performance during the outbreak were below 0.20 in absolute value, except for LNSB (-0.73 ± 0.29). Based on the reaction norm model, estimates of genetic correlations between the intercept and slope terms ranged from 0.24 ± 0.50 to 0.54 ± 0.35 depending on the parameterization used, indicating that selection for the intercept may result in indirect selection for steeper slopes, and thus, less resilient animals. In general, estimates of genetic correlations between farm-year-week effect classes based on the reaction norm model resembled estimates of genetic correlations from the multivariate analysis. Overall, compared to previous studies, antibody S/P ratios showed a lower heritability (0.17 ± 0.05) and low genetic correlations with reproductive performance during a porcine reproductive and respiratory syndrome outbreak, except for the LNSB.

Project description:UnlabelledAs a consequence of their effects on ectodomain shedding, members of the A disintegrin and metalloprotease (ADAM) family have been implicated in the control of various cellular processes. Although ADAM family members are also involved in cancer, inflammation, and other pathologies, it is unclear whether they affect porcine reproductive and respiratory syndrome virus (PRRSV) infection. Here, we demonstrate for the first time that inhibition of ADAM17 enhances PRRSV entry in Marc-145 and porcine alveolar macrophages (PAMs). We also demonstrate that the inhibition of ADAM17 upregulates membrane CD163 expression, a putative PRRSV receptor that is exogenously expressed in BHK-21 and endogenously expressed in Marc-145 and PAMs. Furthermore, overexpression of ADAM17 induced downregulation of CD163 expression and a reduction in PRRSV infection, whereas ablation of ADAM17 expression using specific small interfering RNA resulted in upregulation of CD163 expression with a corresponding increase in PRRSV infection. These ADAM17-mediated effects were confirmed with PRRSV nonpermissive BHK-21 cells transfected with CD163 cDNA. Overall, these findings indicate that ADAM17 downregulates CD163 expression and hinders PRRSV entry. Hence, downregulation of ADAM17 particular substrates may be an additional component of the anti-infection defenses.ImportanceADAM17 is one of the important membrane-associated metalloproteases that mediate various cellular events, as well as inflammation, cancer, and other pathologies. Here, we investigate for the first time the role of the metalloprotease ADAM17 in PRRSV infection. By using inhibitor and genetic modification methods, we demonstrate that ADAM17 negatively regulate PRRSV entry by regulating its substrate(s). More specifically, ADAM 17 mediates the downregulation of the PRRSV cellular receptor CD163. The reduction in CD163 expression represents another component of the anti-infection response initiated by ADAM17.

Dataset Information

Porcine Fc?RI Mediates Porcine Reproductive and Respiratory Syndrome Virus Multiplication and Regulates the Inflammatory Reaction.

Publications

Porcine FcεRI Mediates Porcine Reproductive and Respiratory Syndrome Virus Multiplication and Regulates the Inflammatory Reaction.

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