Porcine reproductive and respiratory syndrome virus infection activates IL-10 production through NF-κB and p38 MAPK pathways in porcine alveolar macrophages

Song, Shuang; Bi, Jing; Wang, Dan; Fang, Liurong; Zhang, Lina; Li, Feng; Chen, Huanchun; Xiao, Shaobo

doi:10.1016/j.dci.2012.10.001

Cited by 77 publications

(50 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Different molecular mechanisms resulting in IL-10 expression are thought to be activated by different stimuli. For example, PRRSV infection was found to activate IL-10 production through the NF-kB (nuclear factor kappa-light-chain-enhancer of activated Bcells) and p38/mitogen-activated protein kinase (MAPK) pathways in porcine alveolar macrophages (Song et al, 2013) and the N protein was involved in NF-kB activation (Luo et al, 2011). Moreover, PRRSV Nsp1 was found to suppress activation of the TNF-a promoter by inhibition of NF-kB and Sp1 (Subramaniam et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Since the transcription factors NF-kB and C/ EBP are involved in the NF-kB pathway, and SP1 is involved in the p38 MAPK pathway, we speculated that the PRRSV N protein may have an effect on the NF-kB, C/EBP or Sp1 elements of the IL-10 promoter. However, this issue will have to be investigated in future studies (Song et al, 2013). were measured with commercial ELISA kits.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The N-N non-covalent domain of the nucleocapsid protein of type 2 porcine reproductive and respiratory syndrome virus enhances induction of IL-10 expression

Liu

Fan

Bai

et al. 2015

Journal of General Virology

View full text Add to dashboard Cite

Porcine reproductive and respiratory syndrome virus (PRRSV) usually establishes a prolonged infection and causes an immunosuppressive state. It has been proposed that IL-10 plays an important role in PRRSV-induced immunosuppression. However, this mechanism has not been completely elucidated. In this study, we found that transfection of 3D4/2 macrophages with the N protein gene of type 2 PRRSV significantly upregulated IL-10 expression at the transcriptional level. Moreover, alanine substitution mutation analysis revealed that the N protein residues 33-37, 65-68 and 112-123 were related to the upregulation of IL-10 promoter activity. Recombinant PRRSV with mutations at residues 33-37 in the N protein (rQ33-5A and rS36A) recovered from corresponding infectious cDNA clones and induced significantly lower levels of IL-10 production in infected monocyte-derived dendritic cells, as compared with their revertants rQ33-5A(R) and rS36A(R), and the wild-type recombinant PRRSV strain rNT/wt. These data indicate that the type 2 PRRSV N protein plays an important role in IL-10 induction and the N-N non-covalent domain is associated with this activity.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The N-N non-covalent domain of the nucleocapsid protein of type 2 porcine reproductive and respiratory syndrome virus enhances induction of IL-10 expression

Liu

Fan

Bai

et al. 2015

Journal of General Virology

View full text Add to dashboard Cite

show abstract

“…Therefore, some viruses, such as Epstein-Barr virus (Samanta et al, 2006), the human immunodeficiency virus (HIV) (Berg et al, 2012) and bovine herpesvirus 1 (da Silva & Jones, 2012), can induce NF-kB activation by the RLR-mediated pathway. In contrast, other viruses such as herpes simplex virus type 1 Takeda et al, 2011), leukaemia virus (Abujamra et al, 2006) and PRRSV (Song et al, 2013) can induce NF-kB activation by the TLR-mediated pathway. By siRNA screening, our studies showed that RIG-I knockdown did not impede PEDV-initiated NF-kB activation; however, silencing the TLR adaptor molecules TRIF and MyD88 clearly impaired PEDV-initiated NF-kB activity (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Total RNA (1 mg) was reverse-transcribed into cDNA in 20 ml reaction volumes. cDNAs were then analysed by real-time RT-PCR using specific primer pairs, as described by Song et al (2013) and Uddin et al (2013). Real-time RT-PCR was performed using a Roche LightCycler 480 Real-Time PCR System, and relative expression levels were evaluated by the 2 2DDCt method (Livak & Schmittgen, 2001).…”

Section: Methodsmentioning

confidence: 99%

Porcine epidemic diarrhea virus infection induces NF-κB activation through the TLR2, TLR3 and TLR9 pathways in porcine intestinal epithelial cells

Cao

Gao

et al. 2015

Journal of General Virology

View full text Add to dashboard Cite

Porcine epidemic diarrhea virus (PEDV) is a coronavirus that induces persistent diarrhoea in swine, resulting in severe economic losses in swine-producing countries. Insights into the interplay between PEDV infection and the innate immune system are necessary for understanding the associated mechanism of pathogenesis. The transcription factor NF-kB plays an important role in regulating host immune responses. Here, we elucidated for the first time to our knowledge the potential mechanism of PEDV-mediated NF-kB activation in porcine small intestinal epithelial cells (IECs). During PEDV infection, NF-kB p65 was found to translocate from the cytoplasm to the nucleus, and PEDV-dependent NF-kB activity was associated with viral dose and active replication. Using small interfering RNAs to screen different mRNA components of the Toll-like receptor (TLR) or RIG-I-like receptor signalling pathways, we demonstrated that TLR2, TLR3 and TLR9 contribute to NF-kB activation in response to PEDV infection, but not RIG-I. By screening PEDV structural proteins for their ability to induce NF-kB activities, we found that PEDV nucleocapsid protein (N) could activate NF-kB and that the central region of N was essential for NF-kB activation. Furthermore, TLR2 was involved in PEDV N-induced NF-kB activation in IECs. Collectively, these findings provide new avenues of investigation into the molecular mechanisms of NF-kB activation induced by PEDV infection.

show abstract

“…Deficiency of TLR4 and 2, produced a significant decrease in the IL-10 production; however the production of this cytokine was almost completely abolished in MyD88-deficient animals ( Figure 6). There is a report that shows MyD88 has an important role in the IL-10 induction during Porcine Reproductive And Respiratory Syndrome Virus (PRRSV) infection [34].…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Innate Immune Cells Induced by Probiotics: Participation of Toll-Like Receptors

C¹

2015

J Clin Cell Immunol

View full text Add to dashboard Cite

Objective: The present work aimed to study the functionality of macrophages from different locations (peritoneum, spleen and Peyer´s patches) when they were stimulated with probiotics microorganisms: Lactobacillus casei CRL 431 and Lactobacillus paracasei CNCM I-1518 or a Probiotic Fermented Milk (PFM) through Toll-Like Receptors (TLRs), prior challenged with agonists or antagonists of TLRs.Methods: BALB/c mice received in the drinking water, the probiotic bacteria (L. casei CRL 431 and L. paracasei CNCM I-1518) or the PFM. We focused our investigation mainly on the phagocytic activity of macrophages from peritoneum, spleen and Peyer's patches and cytokine production were evaluated prior challenged with TLR2 and TLR4 agonists or antagonists. The microbicidal activity of macrophages and against an infection with Salmonella typhimurium was also studied. To assess the role of TLR in probiotic stimulation, we evaluated the phagocytic activity, cytokine production and Immunoglobin G (IgG) anti-OVA in C57BL/6 knockout mice to MyD88, TLR2 and TLR4.Results: In BALB/c mice, the best effect in the phagocytosis assay was obtained with the probiotic bacteria L. casei CRL 431, this effect was reinforced with TLR2 agonist. The production of different cytokines (IL-10 and IL-6) was improved with the probiotic treatments and this production was ameliorated with TLRs agonists. The antimicrobial activity was increased with L. casei CRL 431 and L. paracasei CNCM I-1518, TLR2 and TLR4 antagonists had a negative effect on microbicidal activity. The administration of probiotic bacteria or PFM improved the host response against S. typhimurium controlling the infection during the first hours post-infection. In C57BL/6 knockout mice, phagocytic activity was significantly diminished in comparison to wild type mice and the probiotic bacteria or PFM administration was not able to improve this activity. The IL-10 production was increased at a concentration of 10 8 cells/ml of L. casei CRL 431 in TLR2 -/-and TLR4 -/-, but not in MyD88 -/-mice. The administration of probiotic bacteria or PFM did not play a stimulating effect in the systemic immune response against to OVA antigen in knockout mice. Conclusions:Probiotics modulate the different signaling pathways of innate immune cells through the TLRs. The macrophages activation depends on location of them and that different probiotic strains of Lactobacilli can evoke different intensity of responses. The data suggest that probiotic not only promote a major expression of TLRs but also use these receptors via the innate immune cells as macrophages to stimulate and modulate the immune response.

show abstract

Porcine reproductive and respiratory syndrome virus infection activates IL-10 production through NF-κB and p38 MAPK pathways in porcine alveolar macrophages

Cited by 77 publications

References 35 publications

The N-N non-covalent domain of the nucleocapsid protein of type 2 porcine reproductive and respiratory syndrome virus enhances induction of IL-10 expression

The N-N non-covalent domain of the nucleocapsid protein of type 2 porcine reproductive and respiratory syndrome virus enhances induction of IL-10 expression

Porcine epidemic diarrhea virus infection induces NF-κB activation through the TLR2, TLR3 and TLR9 pathways in porcine intestinal epithelial cells

Stimulation of Innate Immune Cells Induced by Probiotics: Participation of Toll-Like Receptors

Contact Info

Product

Resources

About