About: The combination of PRRS virus and bacterial endotoxin as a model for multifactorial respiratory disease in pigs

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	The combination of PRRS virus and bacterial endotoxin as a model for multifactorial respiratory disease in pigs
Creator	Van Gucht, Steven Labarque, Geoffrey Reeth, Kristien
Source	Elsevier; Medline; PMC
abstract	This paper reviews in vivo studies on the interaction between porcine reproductive and respiratory syndrome virus (PRRSV) and LPS performed in the authors’ laboratory. The main aim was to develop a reproducible model to study the pathogenesis of PRRSV-induced multifactorial respiratory disease. The central hypothesis was that respiratory disease results from an overproduction of proinflammatory cytokines in the lungs. In a first series of studies, PRRSV was shown to be a poor inducer of TNF-α and IFN-α in the lungs, whereas IL-1 and the anti-inflammatory cytokine IL-10 were produced consistently during infection. We then set up a dual inoculation model in which pigs were inoculated intratracheally with PRRSV and 3–14 days later with LPS. PRRSV-infected pigs developed acute respiratory signs for 12–24 h upon intratracheal LPS inoculation, in contrast to pigs inoculated with PRRSV or LPS only. Moreover, peak TNF-α, IL-1 and IL-6 titers were 10–100 times higher in PRRSV–LPS inoculated pigs than in the singly inoculated pigs and the cytokine overproduction was associated with disease. To further prove the role of proinflammatory cytokines, we studied the effect of pentoxifylline, a known inhibitor of TNF-α and IL-1, on PRRSV–LPS induced cytokine production and disease. The clinical effects of two non-steroidal anti-inflammatory drugs (NSAIDs), meloxicam and flunixin meglumine, were also examined. Pentoxifylline, but not the NSAIDs, significantly reduced fever and respiratory signs from 2 to 6 h after LPS. The levels of TNF-α and IL-1 in the lungs of pentoxifylline-treated pigs were moderately reduced, but were still 26 and 3.5-fold higher than in pigs inoculated with PRRSV or LPS only. This indicates that pathways other than inhibition of cytokine production contributed to the clinical improvement. Finally, we studied a mechanism by which PRRSV may sensitize the lungs for LPS. We hypothesized that PRRSV would increase the amount of LPS receptor complex in the lungs leading to LPS sensitisation. Both CD14 and LPS-binding protein, two components of this complex, increased significantly during infection and the amount of CD14 in particular was correlated with LPS sensitisation. The increase of CD14 was mainly due to infiltration of strongly CD14-positive monocytes in the lungs. The PRRSV–LPS combination proved to be a simple and reproducible experimental model for multifactorial respiratory disease in pigs. To what extent the interaction between PRRSV and LPS contributes to the development of complex respiratory disease is still a matter of debate.
has issue date	2004-12-08(xsd:dateTime)
bibo:doi	10.1016/j.vetimm.2004.09.006
bibo:pmid	15507303
has license	no-cc
sha1sum (hex)	20738b294973fa633e5c597a5f8ae426ca673ab9
schema:url	https://doi.org/10.1016/j.vetimm.2004.09.006
resource representing a document's title	The combination of PRRS virus and bacterial endotoxin as a model for multifactorial respiratory disease in pigs
has PubMed Central identifier	PMC7112634
has PubMed identifier	15507303
schema:publication	Vet Immunol Immunopathol
resource representing a document's body	covid:20738b294973fa633e5c597a5f8ae426ca673ab9#body_text
is schema:about of	named entity 'respiratory' named entity 'developed' named entity 'induced' named entity 'IL-10' named entity 'CD14' named entity 'Pentoxifylline' named entity 'develop' named entity 'aim' named entity 'study' named entity 'LPS' named entity 'multifactorial' covid:arg/20738b294973fa633e5c597a5f8ae426ca673ab9 named entity 'mechanism' named entity 'CD14' named entity 'peak' named entity 'non-steroidal anti-inflammatory drugs' named entity 'vivo' named entity 'IL-6' named entity 'inducer' named entity 'pigs' named entity 'signs' named entity 'pigs' named entity 'combination' named entity 'TNF-a' named entity 'inoculated' named entity 'model' named entity 'IL-1' named entity 'LPS-binding protein' named entity 'receptor' named entity 'pathogenesis' named entity 'lungs' named entity 'NSAIDs' named entity 'lungs' named entity 'CD14' named entity 'lungs' named entity 'inoculation' named entity 'cytokine' named entity 'lungs' named entity 'respiratory disease' named entity 'meloxicam' named entity 'LPS' named entity 'pentoxifylline' named entity 'LPS' named entity 'infection' named entity 'respiratory disease' named entity 'LPS' named entity 'LPS' named entity 'respiratory disease' named entity 'studies' named entity 'set' named entity 'PRRSV' named entity 'Van Reeth' named entity 'lungs' named entity 'LPS' named entity 'LPS' named entity 'CD14' named entity 'PRRSV' named entity 'PRRSV' named entity 'asthma' named entity 'pentoxifylline' named entity 'LPS' named entity 'clinical signs' named entity 'P. multocida' named entity 'LPS' named entity 'cytokines' named entity 'LPS-binding protein' named entity 'antibiotics' named entity 'IL-1' named entity 'LPS' named entity 'LPS' named entity 'TNF-a' named entity 'cytokines' named entity 'Lelystad' named entity 'LPS' named entity 'B. bronchiseptica' named entity 'non-steroidal anti-inflammatory drugs' named entity 'influenza virus' named entity 'cytokines' named entity 'IL-10'

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