Molecular mechanisms of decreased steroid responsiveness induced by latent adenoviral infection in allergic lung inflammation

Yamada, Katsuhiko; Elliott, W. Mark; Brattsand, Ralph; Valeur, Anders; Hogg, James C.; Hayashi, Shizu

doi:10.1067/mai.2002.120525

Cited by 32 publications

(28 citation statements)

References 41 publications

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“…Guinea pigs are susceptible to infections by respiratory syncytial virus, influenza virus, parainfluenza virus and adenovirus, each of which having been associated with or used to model exacerbations of asthma and COPD [72,[220][221][222][223][224][225][226][227][228][229][230]. In both humans and in guinea pigs, these infections are characterized by inflammatory cell recruitment (neutrophils, lymphocytes and eosinophils), bronchiolitis, enhanced cytokine gene expression, enhanced responsiveness to experimental challenge (cigarette smoke exposure, allergic inflammation) and airways hyperresponsiveness.…”

Section: Viral Infectionsmentioning

confidence: 99%

Using guinea pigs in studies relevant to asthma and COPD

Canning

Chou

2008

Pulmonary Pharmacology & Therapeutics

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The guinea pig has been the most commonly used small animal species in preclinical studies related to asthma and COPD. The primary advantages of the guinea pig are the similar potencies and efficacies of agonists and antagonists in human and guinea pig airways and the many similarities in physiological processes, especially airway autonomic control and the response to allergen. The primary disadvantages to using guinea pigs are the lack of transgenic methods, limited numbers of guinea pig strains for comparative studies and a prominent axon reflex that is unlikely to be present in human airways. These attributes and various models developed in guinea pigs are discussed.

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Section: Viral Infectionsmentioning

confidence: 99%

Using guinea pigs in studies relevant to asthma and COPD

Canning

Chou

2008

Pulmonary Pharmacology & Therapeutics

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“…As discussed earlier, adenovirus infection in guinea pigs appears to amplify the inflammatory response, but also induces corticosteroid resistance [84]. The steroid resistance may be explained by the reduction in HDAC activity of virusinfected animals [52].…”

Section: Virus Infectionsmentioning

confidence: 99%

Histone acetylation and deacetylation: importance in inflammatory lung diseases

Barnes¹

2005

Eur Respir J

497

350

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Inflammatory lung diseases are characterised by increased expression of multiple inflammatory genes that are regulated by proinflammatory transcription factors, such as nuclear factor-kB. Gene expression is regulated by acetylation of core histones through the action of coactivators, such as CREB-binding protein, with intrinsic histone acetyltransferase (HAT) activity.Conversely, gene repression is mediated via histone deacetylases (HDACs) and other corepressors. In asthma, there is an increase in HAT activity and some reduction in HDAC activity, which is restored by corticosteroid therapy. Corticosteroids switch off inflammatory genes in asthma through the inhibition of HAT activity and by the recruitment of HDAC2 to the activated inflammatory gene complex. In chronic obstructive pulmonary disease, there is a reduction in HDAC2 activity and expression, which may account for the amplified inflammation and resistance to the actions of corticosteroids. The reduction in HDAC2 may be secondary to oxidative and nitrative stress as a result of cigarette smoking and severe inflammation, and may also occur in severe asthma, smoking asthmatic patients and cystic fibrosis.Similar mechanisms may also account for the steroid resistance seen with latent adenovirus infections. The reduction in histone deacetylase activity can be restored by theophylline, which may be able to reverse steroid resistance in chronic obstructive pulmonary disease and other inflammatory diseases.

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“…Thus a reduction in HDAC activity in macrophages [83] may prevent the anti-inflammatory action of corticosteroids, which is dependent on recruitment of HDACs to the inflammatory gene complex [84]. Similarly latent adenovirus appears to induce corticosteroid resistance in experimental animals [242].…”

Section: What Are the Amplifying Mechanisms?mentioning

confidence: 99%

Chronic obstructive pulmonary disease: molecular and cellularmechanisms

Barnes

Shapiro²,

Pauwels³

2003

Eur Respir J

1,231

966

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Chronic obstructive pulmonary disease is a leading cause of death and disability, but has only recently been extensively explored from a cellular and molecular perspective.There is a chronic inflammation that leads to fixed narrowing of small airways and alveolar wall destruction (emphysema). This is characterised by increased numbers of alveolar macrophages, neutrophils and cytotoxic T-lymphocytes, and the release of multiple inflammatory mediators (lipids, chemokines, cytokines, growth factors). A high level of oxidative stress may amplify this inflammation. There is also increased elastolysis and evidence for involvement of several elastolytic enzymes, including serine proteases, cathepsins and matrix metalloproteinases.The inflammation and proteolysis in chronic obstructive pulmonary disease is an amplification of the normal inflammatory response to cigarette smoke. This inflammation, in marked contrast to asthma, appears to be resistant to corticosteroids, prompting a search for novel anti-inflammatory therapies that may prevent the relentless progression of the disease. Eur Respir J 2003; 22: 672-688.

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Molecular mechanisms of decreased steroid responsiveness induced by latent adenoviral infection in allergic lung inflammation

Cited by 32 publications

References 41 publications

Using guinea pigs in studies relevant to asthma and COPD

Using guinea pigs in studies relevant to asthma and COPD

Histone acetylation and deacetylation: importance in inflammatory lung diseases

Chronic obstructive pulmonary disease: molecular and cellularmechanisms

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