Allergic Lung Flashcards
Clinical Features of Bronchial Asthma
1) Acute attacks of SOB; acute airway obstruction b/c of smooth muscle contraction
2) Mucus hypersecretion
3) Airway Inflammation
4) Bronchial hyper-responsiveness
Triggers of Bronchial Asthma
Allergens Chemical Irritants Dust, smoke Cold Post-exercise Psychogenic Post-coughing Post-hyperinflation Post-laughter Viral colds
Inflammation Pathophysiology
-Cytokines
Antigen presentation by dendritic cells leads to Th2 cell response activation.
Th2 cells produce cytokines causing inflammation:
IL-4 causes IgE production
IL-5 activates eosinophils
IL-13 causes mucus secretion and IgE production
IgE Production and Action
IgE produced from B-cells:
first signal from IL-4 or IL-13 and second signal from CD14 on B-cells binding ligand on T-cells
IgE binds to receptors:
1) FCEI on mast cells- high affinity
2) FCEII on lymphocytes, platelets and macrophages- low affinity
Binding leads to mast cell degranulation and inflammatory mediator release
Two Phases of Asthma
Early Phase: bronchoconstriction, mucus hypersecretion, variable vasodilation, increased vascular permeability
Late Phase Reaction: airway inflammation, airflow obstruction, airway hyper-responsiveness
Th1/Th2 Paradigm
Concept that asthma results from polarised T-cell response, in favour of Th2 cells
Factors Affecting the T-cell Phenotype
Factors which favour Th1 cell phenotype: presence of older siblings, early exposure to day care, TB, measles or Hep A infection, rural environment
Factors which favour Th2 cell phenotype: widespread use of antibiotics, western lifestyle, urban environment, diet, sensitisation to house dust-mites and cockroaches