Regulation of endothelin-1 synthesis in cultured guinea pig airway epithelial cells by various cytokines

Endo, Tokiko; Uchida, Yoshiyuki; Matsumoto, Hirokazu; Suzuki, Nobuhiro; Nomura, Akihiro; Hirata, Fusao; Hasegawa, Shizuo

doi:10.1016/s0006-291x(05)81590-6

Cited by 98 publications

(47 citation statements)

References 14 publications

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“…Cutaneous inflammation caused by UVB irradiation is mediated by various cytokines, among which TNF-~ and IL-lct have been thought to be the two major cytokines [22]. The stimulatory effect of TNF-c~ and IL-lc~ on ET-1 expression has been shown in cells of epithelial origin [19,21,31,32]. In this study, we clearly demonstrated that UVB irradiation increases mRNA and secreted protein levels for ET-1 in keratinocytes.…”

Section: Discussionsupporting

confidence: 61%

Ultraviolet B irradiation increases endothelin‐1 and endothelin receptor expression in cultured human keratinocytes

et al. 1995

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The effect of ultraviolet B (UVB) irradiation on endothelin-1 (ET-1) and ET receptor expression was examined using cultured normal human keratinocytes. Keratinocytes secreted ET-1 in the medium at a level of 2.1 pgldayllO s cells. UVB irradiation up to 10 mJIcm z increased ET-1 secretion 3-fold, and potentiated expression of mRNA for ET-1. Both ET A and ET R receptor mRNAs were detected in keratinocytes, and their expression was up-regulated by 5 mJ/cm 2 UVB irradiation.

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Section: Discussionsupporting

confidence: 61%

Ultraviolet B irradiation increases endothelin‐1 and endothelin receptor expression in cultured human keratinocytes

et al. 1995

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“…Various cytokines, which have been shown to be expressed during respiratory tract viral infection (Hennet et al, 1992), induce the release of endothelin-1 from cultured airway epithelial cells (Endo et al, 1992). It has been proposed that increased airway endothelin levels may modulate the expression of endothelin receptors (Henry & Goldie, 1994;Carr et al, 11996).…”

Section: Discussionmentioning

confidence: 99%

Influence of parainfluenza‐1 respiratory tract viral infection on endothelin receptor‐effector systems in mouse and rat tracheal smooth muscle

Knott

Henry

McWilliam

et al. 1996

British J Pharmacology

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1 In this study we have compared the effects of parainfluenza-1 respiratory tract viral infection on the density and function of ETA and ETB receptors in rat and mouse tracheal airway smooth muscle. 2 The bronchoconstrictor effect of inhaled methacholine was significantly enhanced in virus-infected rats, at both 4 and 12 days post-inoculation. That is, the concentration of methacholine causing an increase in resistance of 100% (PC,0o methacholine) was significantly lower in virus-infected animals at both 4 and 12 days post-inoculation (n=6-8; P<0.05). 4 and 12 post-inoculation using the ligands BQ-123 (1 gM; ETA receptor-selective) and sarafotoxin S6c (100 nM; ETB receptor-selective). Total specific binding in mice was significantly reduced at day 2 post-inoculation (n =5; P <0.05) but not at days 4 and 12 post-inoculation (n = 5). In control mice, the proportions of ETA and ETB binding sites were 53%:47% at day 2 and 43%:57% at day 4 and these were significantly altered by parainfluenza-1 infection such that, the ratios were 81%:19% at day 2 and 89%:1 % at day 4 (P<0.05). By day 12 post-inoculation, the proportion of ETA and ETB binding sites in tracheal smooth muscle from mice infected with parainfluenza-1 was not significantly different from control. In rat tracheal airway smooth muscle, neither total specific binding nor the ETA and ETB binding site ratio (64%:36%) were significantly altered in virus-inoculated rats at days 2, 4 or 12 post-inoculation (n = 5). 4 Parainfluenza-1 infection in mice had no effect on the sensitivity or maximal contractile effect of endothelin-1 in tracheal smooth muscle at days 2, 4 or 12 post-inoculation (n = 4). In contrast, contraction in response to the ETB receptor-selective agonist sarafotoxin S6c was attenuated by 39% at day 2 and by 93% at day 4 post-inoculation (P<0.05). However, by day 12 post-inoculation, contractions to sarafotoxin S6c were not significantly different between control and virus-infected mice. In parainfluenza-1-infected rats, there were small but significant reductions in the sensitivity to carbachol, endothelin-1 and sarafotoxin S6c whilst the maximal responses to the highest concentrations of these agonists were not significantly altered by virus infection (n = 8).5 BQ-123 (3 giM) had no significant effect on cumulative concentration-effect curves to endothelin-1 in tracheal preparations from control mice (n =4) or parainfluenza-1-infected rats (n = 8). In contrast, in tissues taken from virus-infected mice at day 4 post-inoculation, BQ-123 caused a marked 9.6 fold rightward shift in the concentration-effect curve to endothelin-1 (n=4).6 In summary, we have demonstrated that parainfluenza-1 infection in mice transiently reduced the density of tracheal airway smooth muscle ETB receptors and this was reflected in reduced responsiveness to the ETB receptor-selective agonist sarafotoxin S6c. In contrast, whilst parainfluenza-l infection in rats was associated with the pathological features and bronchial hyperresponsiveness common to respiratory tract ...

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“…Bronchoconstriction may result from increased synthesis of endothelin -a potent vasoconstrictor and bronchoconstrictor -in response to both cytokines [42]. Furthermore, it is worth mentioning that TNF-α and IL-1 can directly or indirectly alter mucus secretion, ciliary beat frequency and surfactant production in cultured airway epithelial cells (reviewed in [1]).…”

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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Regulation of endothelin-1 synthesis in cultured guinea pig airway epithelial cells by various cytokines

Cited by 98 publications

References 14 publications

Ultraviolet B irradiation increases endothelin‐1 and endothelin receptor expression in cultured human keratinocytes

Ultraviolet B irradiation increases endothelin‐1 and endothelin receptor expression in cultured human keratinocytes

Influence of parainfluenza‐1 respiratory tract viral infection on endothelin receptor‐effector systems in mouse and rat tracheal smooth muscle

Proinflammatory cytokines and viral respiratory disease in pigs

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