Expression of inflammatory cytokines and Toll-like receptors in the brain and respiratory tract of pigs infected with porcine reproductive and respiratory syndrome virus

Miguel, Jennifer C.; Chen, J.; Alstine, William G. Van; Johnson, Rodney W.

doi:10.1016/j.vetimm.2010.01.002

Cited by 31 publications

(19 citation statements)

References 36 publications

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“…Furthermore, infection with RSV results in increased expression of TLR4 mRNA, protein, and increased TLR4 membrane localization [49]. Interestingly, PRRSV infection also induced TLR4 mRNA expression in the brain and respiratory tract of pigs [54]. Thus, it is possible that TLR4 senses one or more proteins encoded by PRRSV to induce an inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Porcine Reproductive and Respiratory Syndrome Virus Induces IL-1βProduction Depending on TLR4/MyD88 Pathway and NLRP3 Inflammasome in Primary Porcine Alveolar Macrophages

Song

Fang

et al. 2014

Mediators of Inflammation

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Porcine reproductive and respiratory syndrome virus (PRRSV) is an Arterivirus that has been devastating the swine industry worldwide since the late 1980s. Previous studies have reported that PRRSV infection induced the production of IL-1β. However, the cellular sensors and signaling pathways involved in this process have not been elucidated yet. Here, we studied the mechanisms responsible for the production of IL-1β in response to highly pathogenic PRRSV. Upon PRRSV infection of primary porcine alveolar macrophages, both mRNA expression and secretion of IL-1β were significantly increased in a time- and dose-dependent manner. We also investigated the role of several pattern-recognition receptors and adaptor molecules in this response and showed that the TLR4/MyD88 pathway and its downstream signaling molecules, NF-κB, ERK1/2, and p38 MAPKs, were involved in IL-1β production during PRRSV infection. Treatment with specific inhibitors or siRNA knockdown assays demonstrated that components of the NLRP3 inflammasome were crucial for IL-1β secretion but not for IL-1β mRNA expression. Furthermore, TLR4/MyD88/NF-κB signaling pathway was involved in PRRSV-induced expression of NLRP3 inflammasome components. Together, our results deciphered the pathways leading from recognition of PRRSV to the production and release of IL-1β, providing a deeper knowledge of the mechanisms of PRRSV-induced inflammation responses.

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Section: Discussionmentioning

confidence: 99%

Porcine Reproductive and Respiratory Syndrome Virus Induces IL-1βProduction Depending on TLR4/MyD88 Pathway and NLRP3 Inflammasome in Primary Porcine Alveolar Macrophages

Song

Fang

et al. 2014

Mediators of Inflammation

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“…In pigs infected with porcine reproductive and respiratory syndrome virus, TLR4 is up-regulated in tracheobronchial lymph node, brain, hypothalamus, hippocampus and, to a lesser extent, in the cortex and cerebellum. But it is not up-regulated in the lungs (95). …”

Section: Molecular Cellular and Functional Properties Of Tlr4 Acrosmentioning

confidence: 99%

A Comparative Review of Toll-Like Receptor 4 Expression and Functionality in Different Animal Species

2014

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Toll-like receptors (TLRs) belong to the pattern recognition receptor (PRR) family, a key component of the innate immune system. TLRs detect invading pathogens and initiate an immediate immune response to them, followed by a long-lasting adaptive immune response. Activation of TLRs leads to the synthesis of pro-inflammatory cytokines and chemokines and the expression of co-stimulatory molecules. TLR4 specifically recognizes bacterial lipopolysaccharide, along with several other components of pathogens and endogenous molecules produced during abnormal situations, such as tissue damage. Evolution across species can lead to substantial diversity in the TLR4’s affinity and specificity to its ligands, the TLR4 gene and cellular expression patterns and tissue distribution. Consequently, TLR4 functions vary across different species. In recent years, the use of synthetic TLR agonists as adjuvants has emerged as a realistic therapeutic goal, notably for the development of vaccines against poorly immunogenic targets. Given that an adjuvanted vaccine must be assessed in pre-clinical animal models before being tested in humans, the extent to which an animal model represents and predicts the human condition is of particular importance. This review focuses on the current knowledge on the critical points of divergence between human and the mammalian species commonly used in vaccine research and development (non-human primate, mouse, rat, rabbit, swine, and dog), in terms of molecular, cellular, and functional properties of TLR4.

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“…Several ones reported that PRRSV could suppress TNF-␣ production (Genini et al, 2008;Subramaniam et al, 2010;Thanawongnuwech et al, 2004;Van Reeth et al, 1999), while some literatures showed that TNF-␣ in PRRSV-infected PAMs and increased level of TNF-␣ in serum could be detected (Choi and Chae, 2002;Miguel et al, 2010). Recent study concluded that different PRRSV isolates had ability to induce different patterns of TNF-␣ (Gimeno et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

“…In PRRSV, previous studies seemed to be controversial on the induction of TNF-␣ upon infection. Few studies showed that PRRSV can suppress TNF-␣ production both in vitro and in vivo (Genini et al, 2008;Subramaniam et al, 2010;Thanawongnuwech et al, 2004;Van Reeth et al, 1999); others showed a detectable TNF-␣ in PRRSV-infected PAMs (Choi and Chae, 2002), and an increased TNF-␣ mRNA in the tracheobronchial lymph nodes and an elevated level of TNF-␣ in serum (Miguel et al, 2010). Additionally, the increased pro-inflammatory cytokines have also been observed in co-infection models of PRRSV with other pathogens (Shi et al, 2010;Van Gucht et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Both Nsp1β and Nsp11 are responsible for differential TNF-α production induced by porcine reproductive and respiratory syndrome virus strains with different pathogenicity in vitro

Zhou

et al. 2015

Virus Research

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Expression of inflammatory cytokines and Toll-like receptors in the brain and respiratory tract of pigs infected with porcine reproductive and respiratory syndrome virus

Cited by 31 publications

References 36 publications

Porcine Reproductive and Respiratory Syndrome Virus Induces IL-1βProduction Depending on TLR4/MyD88 Pathway and NLRP3 Inflammasome in Primary Porcine Alveolar Macrophages

Porcine Reproductive and Respiratory Syndrome Virus Induces IL-1βProduction Depending on TLR4/MyD88 Pathway and NLRP3 Inflammasome in Primary Porcine Alveolar Macrophages

A Comparative Review of Toll-Like Receptor 4 Expression and Functionality in Different Animal Species

Both Nsp1β and Nsp11 are responsible for differential TNF-α production induced by porcine reproductive and respiratory syndrome virus strains with different pathogenicity in vitro

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