Interleukin-1?-induced neutrophil recruitment and acute lung injury in hamsters

Patton, Lavonne M.; Saggart, Betty S.; Ahmed, Nahed K.; Leff, Jonathan A.; Repine, John E.

doi:10.1007/bf01534377

Cited by 30 publications

(20 citation statements)

References 17 publications

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“…In contrast, the extent of tissue damage in endotoxintreated mice, a model for sepsis-induced ARDS, was reduced by treatment with TNF-␣ antagonists. These results suggest that TNF-␣ may play an important role in lung injury induced by bacterial lipopolysaccharide (LPS), supporting a potential role for these cytokines at least in sepsis-induced ARDS (22,24,26,32), but may play less of a role in reovirus 1/L-induced ARDS as well as ARDS due to trauma or severe hemorrhage (21,25). However, whether the concentration of individual cytokines/chemokines is of a predictive value for either the development of or the recovery from ARDS remains controversial (1).…”

Section: Discussionmentioning

confidence: 97%

Respiratory Reovirus 1/L Induction of Diffuse Alveolar Damage: Pulmonary Fibrosis Is Not Modulated by Corticosteroids in Acute Respiratory Distress Syndrome in Mice

London

Majeski

Altman-Hamamdzic

et al. 2002

Clinical Immunology

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Section: Discussionmentioning

confidence: 97%

Respiratory Reovirus 1/L Induction of Diffuse Alveolar Damage: Pulmonary Fibrosis Is Not Modulated by Corticosteroids in Acute Respiratory Distress Syndrome in Mice

London

Majeski

Altman-Hamamdzic

et al. 2002

Clinical Immunology

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“…However, IL-1b is a direct product of LPS-dependent activation of the TLR4 pathway, and IL-1b gene expression has been identified as a common thread in multiple models of ventilator-induced lung injury. IL-1b causes neutrophil recruitment and injury in the lungs of hamsters (34,35), and there is evidence that early inflammatory responses in the lungs of humans with ARDS are predominantly attributable to IL-1b and not to IL-6 or TNF-a (36,37).…”

Section: Discussionmentioning

confidence: 99%

Effects of Age on the Synergistic Interactions between Lipopolysaccharide and Mechanical Ventilation in Mice

Smith

Gharib

Frevert

et al. 2010

Am J Respir Cell Mol Biol

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Children have a lower incidence and mortality from acute lung injury (ALI) than adults, and infections are the most common event associated with ALI. To study the effects of age on susceptibility to ALI, we investigated the responses to microbial products combined with mechanical ventilation (MV) in juvenile (21-d-old) and adult (16-wk-old) mice. Juvenile and adult C57BL/6 mice were treated with inhaled Escherichia coli 0111:B4 lipopolysaccharide (LPS) and MV using tidal volume 5 15 ml/kg. Comparison groups included mice treated with LPS or MV alone and untreated age-matched control mice. In adult animals treated for 3 hours, LPS plus MV caused synergistic increases in neutrophils (P , 0.01) and IgM in bronchoalveolar lavage fluid (P 5 0.03) and IL-1b in whole lung homogenates (P , 0.01) as compared with either modality alone. Although juvenile and adult mice had similar responses to LPS or MV alone, the synergistic interactions between LPS and MV did not occur in juvenile mice. Computational analysis of gene expression array data suggest that the acquisition of synergy with increasing age results, in part, from the loss of antiapoptotic responses and the acquisition of proinflammatory responses to the combination of LPS and MV. These data suggest that the synergistic inflammatory and injury responses to inhaled LPS combined with MV are acquired with age as a result of coordinated changes in gene expression of inflammatory, apoptotic, and TGF-b pathways.

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“…In vivo, the TNF-α/IL-1 associated neutrophilic exudate has been linked to an increased phagocytic capacity of the lung, with release of enzymes from neutrophils and with respiratory burst activity. The local release of enzymes from neutrophils probably makes important contributions to lung tissue injury and increased vascular permeability with resultant lung haemorrhages and edema [94,129]. In vitro studies have demonstrated stimulating effects of TNF-α and IL-1 on both neutrophils and macrophages of several animal species.…”

Section: Cytokine Effects On the Respiratory Tractmentioning

confidence: 99%

Proinflammatory cytokines and viral respiratory disease in pigs

2000

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-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...

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Interleukin-1?-induced neutrophil recruitment and acute lung injury in hamsters

Cited by 30 publications

References 17 publications

Respiratory Reovirus 1/L Induction of Diffuse Alveolar Damage: Pulmonary Fibrosis Is Not Modulated by Corticosteroids in Acute Respiratory Distress Syndrome in Mice

Respiratory Reovirus 1/L Induction of Diffuse Alveolar Damage: Pulmonary Fibrosis Is Not Modulated by Corticosteroids in Acute Respiratory Distress Syndrome in Mice

Effects of Age on the Synergistic Interactions between Lipopolysaccharide and Mechanical Ventilation in Mice

Proinflammatory cytokines and viral respiratory disease in pigs

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