Asthma
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| show | Chronic inflammation condition, airflow limitation, tissue remodelling
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| show | allergic disease/ tobacco smoke and irritants
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| show | Reversible airflow obstruction/ incompletely reversible airflow limitation, resulting in progressive decline of lung function
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| Classical pathlogies | show 🗑
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| show | neutrophilic (IL-17A)
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| show | eosinophilic
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| Inflammatory response in asthma | show 🗑
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| show | Th1-dominated responses: IFNgmma, IL-8 (neutrophil chemoat.) leukotriene B4, IL-1 and TNFa (which induce asthma via IL-4, IL-5 and IL-13)
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| show | Inflammatory characteristics of asthma and COPD are interchangeable during exacerbation and infection, due to the association with the similar cytokine profiles and levels
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| Asthma pathology | show 🗑
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| Asthma - initiation | show 🗑
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| Asthma - T cell co-stimulation | show 🗑
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| show | CD25+ FOXP3+ T cell is suggested to control Th2 through IL-10 and TGFbeta
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| Central mediator of allergic response (atopic form asthma) - IgE | show 🗑
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| Upon subsequent antigen exposure | show 🗑
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| Then move on the the later allergic response (6-72 hrs later) | show 🗑
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| show | prominent in allergic airway disease, linked asthma severity
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| show | 1)release of pre-stored granular proteins e.g. e- cationic proteins and e-peroxidase, which are cytotoxic 2)synthesis and release of oxygen radicals and lipid mediators as well as numerous cytokines 3)role in airway remodelling: fibrogenic cytokines
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| show | produced by Th2, mast cell and eosinophil, regulate most aspects of eosinophil behaviour
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| show | 1)collagen 2)fibronectin deposition 3)thinkness of subepithelial basement membrane 4)goblet cell hyperplasia 5)increased ASM mass and size 6)angiogenesis 7)fibrosis
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| show | imbalance of matrix metalloproteinases and their inhibitors, also increase in ASM content, along with change in the phenotype of fibroblasts cause permanent reduction of airway caliber, which is steroid insensitive
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| Airway remodelling - associated cytokines | show 🗑
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| show | 1)on eosinophil survival by prevent the release of chemoattractants 2)downregulation of IL-4, which induces isotype switching of B cell, 3)inhibit IFNgamma and IL-2,4)interfere with function of mono and Macro, 5) MHC expression on APCs
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| show | class CC, target T cells, monocytes and eosinophils. Eotaxin and RANTES, acting in synergy with IL-5, chemoattractant in allergic inflammation, induce A4 and B1 integrin expression on eosinphil- firm adhesion to epitheilium and tranmigration
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| Therapies - 1 | show 🗑
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| show | interacts with co-activators with HAT activity, which activate pro-in transcription factors wuch as NFkB and AP1
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| show | IL-10 and IkB-alpha
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| Ineffective in virus-induced exacerbation and COPD | show 🗑
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| Therapies - 2 | show 🗑
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| actions | show 🗑
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| show | Immunotherapy, increase the production of IgA and IgG, Treg cell (TGFbeta adn IL-10), reduction in the recruitment of Macro B and E-phil
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| Therapies - 4 | show 🗑
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| Therapies - 5 | show 🗑
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| Therapies - 6 | show 🗑
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| show | Inhaled cigarette smoke and other irritants activates epithelial cells and Macrophage to release chemotactic factors
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| show | CCL2 on CCR2 monocytes, CXCL1 and CXCL8 on CCR2 neutrophils and monocytes, CXCL9, CXCL10, CXCL11 on CCR3 Th1 and Tc1 cells
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| COPD - pathology | show 🗑
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| show | release TGFbeta, which stimulates fibroblast proliferation, resulting in fibrosis in small airways
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| show | B2 agonist
theophylline (PDE inhibitor, increasing cAMP)
Muscarinic receptor antagonist
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| other approaches for both | show 🗑
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