The release of leukotrienes in the respiratory tract during infection with respiratory syncytial virus: Role in obstructive airway disease

Volovitz, Benjamin; Welliver, Robert C.; Castro, G. De

doi:10.1016/0883-9441(89)90079-8

Cited by 47 publications

(75 citation statements)

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“…Indeed, COX-2 Ϫ/Ϫ mice have markedly lower levels of the prototypic Th1 cytokine IFN-␥ in BAL fluid after infection. Alternatively, the enhanced levels of cysteinyl LTs may be a reflection of the enhanced viral titers in the lungs of the COX-2 Ϫ/Ϫ mice as respiratory viral infection is associated with elevated LT levels (41,45).…”

Section: Discussionmentioning

confidence: 99%

Contrasting Effects of Cyclooxygenase-1 (COX-1) and COX-2 Deficiency on the Host Response to Influenza A Viral Infection

Carey¹,

Bradbury²,

Seubert³

et al. 2005

The Journal of Immunology

102

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Influenza is a significant cause of morbidity and mortality worldwide despite extensive research and vaccine availability. The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. We used an influenza A viral infection model in wild type (WT), COX-1−/−, and COX-2−/− mice. Infection induced less severe illness in COX-2−/− mice in comparison to WT and COX-1−/− mice as evidenced by body weight and body temperature changes. Mortality was significantly reduced in COX-2−/− mice. COX-1−/− mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2−/− mice. However, lung viral titers were markedly elevated in COX-2−/− mice relative to WT and COX-1−/− mice on day 4 of infection. Levels of PGE2 were reduced in COX-1−/− airways whereas cysteinyl leukotrienes were elevated in COX-2−/− airways following infection. Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.

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Section: Discussionmentioning

confidence: 99%

Contrasting Effects of Cyclooxygenase-1 (COX-1) and COX-2 Deficiency on the Host Response to Influenza A Viral Infection

Carey¹,

Bradbury²,

Seubert³

et al. 2005

The Journal of Immunology

102

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“…Furthermore, the fact that hypertonic saline causes a variety of symptoms even in normal subjects, leads to the speculation that it mimics some functional effects occurring during exacerbations in COPD. Leukocytes from patients with COPD are capable of releasing significant amounts of leukotrine C 4 upon stimulation [28] and cysteinyl leukotrienes are produced in response to viral infections [29], as one potential factor in exacerbations. Given that, the airway response to hypertonic saline could be an acute model of the functional although not immunological processes that are acting during exacerbations in COPD.…”

Section: Discussionmentioning

confidence: 99%

Montelukast attenuates the airway response to hypertonic saline in moderate-to-severe COPD

Zühlke

Kanniess²,

Richter³

et al. 2003

European Respiratory Journal

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This study assessed the effect of the leukotriene receptor antagonist montelukast on hypertonic saline-induced airway obstruction.A total of 29 patients with chronic obstructive pulmonary disease (forced expiratory volume in one second (FEV1), 42 ¡ 4% predicted) received either 10 mg montelukast and 3 h later placebo via metered-dose inhaler (MDI) (M), or placebo and 3h later 200 mg salbutamol (S), or two doses of placebo (P), in a randomised order. Patients inhaled salbutamol 1 h after MDI and the challenge was performed 15 min later (3% saline, 5 min). Data are given as per cent changes versus baseline.Compared to P, S caused significant bronchodilation in FEV1 (7.3%) and forced inspiratory volume in one second (FIV1) (4.5%), and M in FIV1 (1.5%). The salineinduced fall in FEV1 was lower after M (-5.8%), compared with S (-10.3%) and P (-13.1%). FEV1 (11.3%) and FIV1 (7.6%) was improved over baseline after recovery by M but not P and S. Recovery times regarding FEV1 (8.5 min) and FIV1 (15.2 min) were shortest after M, respective values for S being 16.8 and 20.4 min, and for P 15.9 and 21.2 min. Effects were strongest in patients with low baseline FEV1 and/or inhaled corticosteroids.Data from this study indicate beneficial effects of montelukast on hypertonic salineinduced airway responses in patients with chronic obstructive pulmonary disease, particularly those with severe disease. The major effect was an accelerated recovery leading to values above baseline. Eur Respir J 2003; 22: 926-930.

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“…Cytokines and chemokines, such as interleukin (IL)-8 and regulated on activation, normal T-cell expressed and secreted (RANTES) increase in airway secretions during viral infections and recruit and activate inflammatory cells such as neutrophils, eosinophils and activated T-cells that have all been linked to asthma [1]. Consequently, elevated levels of eosinophil cationic protein and cysteinyl leukotrienes are found in nasal secretions from infants with RSV infection [27][28][29]. Elevations are particularly pronounced in bronchiolitis [27,30].…”

Section: Respiratory Syncytial Virus-induced Inflammationmentioning

confidence: 99%

Relationship between respiratory syncytial virus bronchiolitis and future obstructive airway diseases

Wennergren¹,

Kristjánsson²

2001

European Respiratory Journal

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Relationship between respiratory syncytial virus bronchiolitis and future obstructive airway diseases. G. Wennergren, S. Kristjánsson. #ERS Journals Ltd 2001. ABSTRACT: Evidence from a large number of prospective case-control studies shows that respiratory syncytial virus (RSV) bronchiolitis in infancy is often associated with recurrent wheezing and asthma during subsequent years. However, wheezing tends to diminish and most studies show no significant increase in wheezing compared to controls by school age or adolescence. An unresolved question is whether severe RSV infection during infancy causes the respiratory sequelae or inherent abnormalities predispose an infant to develop severe respiratory infection and sequelae, i.e. RSV is associated with the development of pulmonary sequelae.Studies on long-term outcome of RSV bronchiolitis are reviewed from an evidencebased perspective.The majority of prospective placebo-controlled studies do not show any long-term beneficial effects of corticosteroid treatment, i.e. the risk of subsequent wheezing is not diminished by the treatment. The evidence for an increased risk of allergic sensitization after RSV bronchiolitis is not nearly as strong as the evidence for an increased risk of subsequent wheezing. In fact, most studies do not show any significant increase in atopy after RSV bronchiolitis. This suggests that the increased risk of wheezing after RSV is not linked to an increased risk of atopy. There are some indications that infants who develop severe RSV and subsequent wheezing may have aberrations that predate the RSV infection.To decide whether respiratory syncytial virus bronchiolitis causes, or is associated with the respiratory sequelae (or with subsequent allergy), it will be necessary to conduct prospective, randomized studies, where the cytokine profile prior to bronchiolitis onset is known. Such studies should preferably include some form of intervention against respiratory syncytial virus. A more complete understanding of the risk factors for severe respiratory syncytial virus infection and the role of respiratory syncytial virus infection in the initiation of asthma is needed as a basis for large-scale and cost-effective programmes to prevent respiratory syncytial virus-related morbidity. Eur Respir J 2001; 18: 1044-1058. Respiratory syncytial virus (RSV) bronchiolitis is the most common, severe lower respiratory tract infection in infancy. It now seems well established that RSV bronchiolitis in infancy is associated with recurrent wheezing and asthma during the first decade of life. In some children, wheezing after early lower airway infection with RSV is transient, but in many of the children RSV-induced bronchiolitis represents the onset of asthma. In fact, there are results which indicate that severe RSV bronchiolitis in the young infant may shift the T-helper (Th)1/Th2 balance in favour of a Th2 cytokine pattern, leading to development of allergic sensitization and persistent asthma [1,2]. However, the association with risk of development of atopy...

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The release of leukotrienes in the respiratory tract during infection with respiratory syncytial virus: Role in obstructive airway disease

Cited by 47 publications

References 0 publications

Contrasting Effects of Cyclooxygenase-1 (COX-1) and COX-2 Deficiency on the Host Response to Influenza A Viral Infection

Contrasting Effects of Cyclooxygenase-1 (COX-1) and COX-2 Deficiency on the Host Response to Influenza A Viral Infection

Montelukast attenuates the airway response to hypertonic saline in moderate-to-severe COPD

Relationship between respiratory syncytial virus bronchiolitis and future obstructive airway diseases

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