Production of interleukin 1 and tumour necrosis factor activities in bronchoalveolar washings following infection of mice by influenza virus

Vacheron, F; Rudent, A.; Perin, S.; Labarre, C; Quero, A.M.; Guenounou, M.

doi:10.1099/0022-1317-71-2-477

Cited by 65 publications

(30 citation statements)

References 12 publications

(14 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Type I IFNs (IFN-␣/␤) are the key cytokines produced by influenza A virus-infected epithelial cells, monocytes/macrophages, and spleen cells (5,29,39,52,54,70) and function as antiviral factors. Several studies have demonstrated that an early rise in the levels of IFN-␣, tumor necrosis factor (TNF), IL-1␣, IL-1␤, and IL-6 in bronchoalveolar lavage fluids or lung homogenates is associated with symptom development and lung pathology in influenza virus-infected mice (19,33,47,69). Therefore, the levels of IL-6 and IFN-␣ in serum samples and lungs of the mutant virus-infected mice were determined.…”

Section: Resultsmentioning

confidence: 99%

Mutations in Influenza Virus M1 CCHH, the Putative Zinc Finger Motif, Cause Attenuation in Mice and Protect Mice against Lethal Influenza Virus Infection

Hui¹,

Smee

Wong

et al. 2006

J Virol

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 99%

Mutations in Influenza Virus M1 CCHH, the Putative Zinc Finger Motif, Cause Attenuation in Mice and Protect Mice against Lethal Influenza Virus Infection

Hui¹,

Smee

Wong

et al. 2006

J Virol

View full text Add to dashboard Cite

“…Until now, the association between cytokines and influenza pneumonia has been studied exclusively in mice, which are not natural influenza virus hosts. In this murine model, there is an early increase of both TNF-α and IL-1 [59,99,131] in bronchoalveolar lavage fluids (BAL), and cytokines correlate with the characteristic signs of disease (lethargy, anorexia, followed by mortality) and with mononuclear cell infiltration in the lungs and gross lesion development. In a study by Hennet et al [59], production of TNF-α/IL-1 was followed by that of other cytokines and inflammatory products: IL-6, granulocyte macrophage-colony stimulating factor, IFN-γ and leukotriene B4.…”

Section: Cytokines In Viral Respiratory Diseases Of Humansmentioning

confidence: 99%

Proinflammatory cytokines and viral respiratory disease in pigs

2000

View full text Add to dashboard Cite

-Swine influenza virus (SIV), porcine respiratory coronavirus (PRCV) and porcine reproductive and respiratory syndrome virus (PRRSV) are enzootic viruses causing pulmonary infections in pigs. The first part of this review concentrates on known clinical and pathogenetic features of these infections. SIV is a primary respiratory pathogen; PRCV and PRRSV, on the contrary, tend to cause subclinical infections if uncomplicated but they appear to be important contributors to multifactorial respiratory diseases. The exact mechanisms whereby these viruses cause symptoms and pathology, however, remain unresolved. Classical studies of pathogenesis have revealed different lung cell tropisms and replication kinetics for each of these viruses and they suggest the involvement of different lung inflammatory responses or mediators. The proinflammatory cytokines interferon-α (IFN-α), tumour necrosis factor-α (TNF-α) and interleukin-1 (IL-1) have been shown to play key roles in several respiratory disease conditions. The biological effects of these cytokines and their involvement in human viral respiratory disease are discussed in the second part of this review. The third part summarises studies that were recently undertaken in the authors' laboratory to investigate the relationship between respiratory disease in pigs and bioactive lung lavage levels of IFN-α, TNF-α and IL-1 during single and combined infections with the above viruses. In single SIV infections, typical signs of swine "flu" were tightly correlated with an excessive and coordinate production of the 3 cytokines examined. PRCV or PRRSV infections, in contrast, were subclinical and did not induce production of all 3 cytokines. Combined infections with these 2 subclinical respiratory viruses failed to potentiate disease or cytokine production. After combined inoculation with PRCV followed by bacterial lipopolysaccharide, both clinical respiratory disease and TNF-α/IL-1 production were markedly more severe than those associated with the respective single inoculations. Taken together, these data are the first to demonstrate that proinflammatory cytokines can be important mediators of viral respiratory diseases in pigs. respiratory coronavirus, PRCV), et le virus du syndrome dysgénésique et respiratoire porcin (porcine reproductive and respiratory syndrome virus, PRRSV) sont des virus enzootiques provoquant des infections pulmonaires chez le porc. Les caractéristiques cliniques et pathogénétiques de ces infections sont données dans la première partie de cette revue. Le SIV est un agent pathogène respiratoire primaire ; les PRCV et PRRSV, en revanche, ne causent que des infections subcliniques en l'absence de complications, mais ils contribuent de manière importante aux maladies respiratoires multifactorielles. Cependant, les mécanismes précis par lesquels ces virus provoquent des symptômes et une pathologie demeurent inconnus. Les études classiques de pathogenèse ont révélé un tropisme pour les cellules pulmonaires et des cinétiques de réplication différents pour...

show abstract

“…Various independent research groups have reported increase in IFNα, TNF-α, IL-1 α and β and IL-6 levels in Bronchoalveolar Lavage (BAL) fluid or lung homogenates ( Figure 1) after intranasal infection of mice with A/PR/ 8/34 [29][30][31][32]. Treatment of virus infected mice with antibodies to the cytokine have been reportedly associated with IFN-α and IL-1α.…”

Section: In Vivo Modelsmentioning

confidence: 99%

Influenza virus Induced Cytokine Responses: An Evaluation of Host-Pathogen Association

2014

Immunome Res

View full text Add to dashboard Cite

Influenza is an acute viral infection of the respiratory tract and there are many reports suggesting that many of the clinical and pathological manifestations of influenza virus are due to various cytokines. These proteins act as chemical messengers and aid in viral clearance and cell death, such as, interferon-a (IFN-α), tumour necrosis factora (TNF-α), interleukin-1 (IL-1) α and β, interleukin-6 (IL-6), interleukin-8 (IL-8) and monocyte-attracting chemokines. Cytokine gene expression leads to activation of NF-ĸB, AP-1, STAT and IRF signal transducing molecules in influenza A virus-infected cells. Anti-viral defence mediated by influenza A virus-induced IFN-α/β have proved to be very essential. IFN-α/β is known to prolong T cell survival, upregulate IL-12 and IL-18 receptor gene expression and together with IL-18 stimulate NK and T cell IFN-γ production and the development of Th1-type immune response. It has been observed, though, not completely understood, that the cytokine responses differ depending on the type of host. This review aims to give a composed account of the cytokine/ chemokine responses, with special reference to the differences observed in various host-virus combinations.

show abstract

Production of interleukin 1 and tumour necrosis factor activities in bronchoalveolar washings following infection of mice by influenza virus

Cited by 65 publications

References 12 publications

Mutations in Influenza Virus M1 CCHH, the Putative Zinc Finger Motif, Cause Attenuation in Mice and Protect Mice against Lethal Influenza Virus Infection

Mutations in Influenza Virus M1 CCHH, the Putative Zinc Finger Motif, Cause Attenuation in Mice and Protect Mice against Lethal Influenza Virus Infection

Proinflammatory cytokines and viral respiratory disease in pigs

Influenza virus Induced Cytokine Responses: An Evaluation of Host-Pathogen Association

Contact Info

Product

Resources

About