By Jan Lotvall
content material: Similarities and modifications within the pathophysiology of bronchial asthma and COPD / Christian Virchow --
Glucocorticoids : pharmacology and mechanisms / Peter Barnes --
Inhaled corticosteroids? scientific results in bronchial asthma and COPD / Paul O'Byrne --
LABAS : pharmacology, mechanisms and interplay with anti inflammatory remedies / Gary Anderson --
lengthy and ultra-long appearing beta-2-agonists / Mario Cazzola --
the protection of long-acting beta agonists and the improvement of mixture remedies for bronchial asthma and protracted obstructive pulmonary illness / Eugene Bleecker --
Inhaled mix remedy with glucocorticoids and long-acting beta-2-agonists in bronchial asthma and COPD, present and destiny views / Jan Lotvall --
Novel anti inflammatory remedies for bronchial asthma and COPD / Ian Adcock --
Novel biologicals by myself and together in bronchial asthma and hypersensitivity / William Busse --
Anti-infective remedies in bronchial asthma and COPD / Jonathan D.R. Macintyre & Sebastian L. Johnston --
lengthy appearing muscarinic antagonists in bronchial asthma and COPD / Denis O'Donnell --
Phosphodiesterase inhibitors in obstructive lung sickness / Jan Lotvall --
organic remedies in improvement for COPD / Riccardo Polosa --
Triple therapy?, within the administration of power obstructive lung disorder (COPD). the worth of mixture remedy with inhaled steroid, lengthy performing anticholinergicbronchodilator and lengthy appearing beta 2 agonist bronchodilator in COPD / Ronald Dahl.
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Extra info for Advances in combination therapy for asthma and COPD
Reproduced with permission from Adcock IM, Ito K, Barnes PJ. Histone deacetylation: an important mechanism in inﬂammatory lung diseases. COPD 2005;2(4):445–455. P1: OTA/XYZ JWST083-03 P2: ABC JWST083-L¨otvall September 8, 2011 0:47 Printer Name: Yet to Come INHALED CORTICOSTEROIDS: CLINICAL EFFECTS IN ASTHMA AND COPD 41 function in patients thought to have a component of ﬁxed airﬂow obstruction, or in patients with a predominantly peripheral lung disease such as sarcoidosis. Corticosteroids, such as prednisone or methylprednisolone, are rapidly and completely absorbed across the gastrointestinal tract and thus have a very high oral bioavailability.
51 This presumably means that glucocorticoids are not able to activate certain genes that are critical to the anti-inﬂammatory action of high doses of glucocorticoids, but whether this is a rare genetic defect is not yet known. 8 Proposed mechanism of glucocorticoid resistance in COPD, severe asthma and smoking asthma. Stimulation of normal and asthmatic alveolar macrophages activates nuclear factor-B (NF-B) and other transcription factors to switch on histone acetyltransferase leading to histone acetylation and subsequently to transcription of genes encoding inﬂammatory proteins, such as tumour necrosis factor-␣ (TNF-␣), interleukin-8 (IL-8) and granulocyte-macrophage colony stimulating factor (GM-CSF).
Histone acetylation affects gene transcription and is controlled by histone acetyltransferases (HATs). 6 Thus, inﬂammatory genes, activated by inﬂammatory stimuli, result in increased levels of I-B kinase-2 (IKK2), which in turn activates NF-B. This results in acetylation of lysines in core histone H4, resulting in increased expression of genes encoding proinﬂammatory proteins. After activation by corticosteroids, GRs translocate to the nucleus and bind to coactivators to directly inhibit HAT activity, and histone deacetylases (HDAC) are recruited.