Asthma Flashcards
anti-inflammatory cytokines;
may be deficient in asthma
IL-10 and IL-12
anti-inflammatory cytokines;
may be deficient in asthma
IL-10 and IL-12
upstream cytokine released from epithelial cells of asthmatics that orchestrates the release of chemokines that selectively attract TH2 cells
Thymic stromal lymphopoietin
selectively attractant to eosinophils via CCR3 and is expressed by epithelial cells of asthmatics
Eotaxin
CCL11
expressed by epithelial cells of asthmatics attract TH2 cells via CCR4
CCL17 (TARC) and CCL22 (MDC)
expressed by epithelial cells of asthmatics attract TH2 cells via CCR4
CCL17 (TARC) and CCL22 (MDC)
Proinflammatory transcription factors activated in asthmatic airways
nuclear factor-B (NF-B)
activator protein-1
Proinflammatory transcription factors activated in asthmatic airways
nuclear factor-B (NF-B)
activator protein-1
transcription factors regulate the expression of TH2 cytokines in T cells
nuclear factor of activated T cells
GATA-3
transcription factors regulate the expression of TH2 cytokines in T cells
nuclear factor of activated T cells
GATA-3
Bronchoconstrictor mediators released in asthma
Chemokines
Histamines
Leukotrienes
Prostaglandin D2
physiologic abnormality of asthma:
Airway hyperresponsiveness
Bronchoconstrictor mediators released in asthma
histamine, prostaglandin D2, Cysteinyl leukotrienes, cytokines, chemokines, growth factors, neutrotropins
physiologic abnormality of asthma:
Airway hyperresponsiveness
Mech for basement membrane thickening in asthmatic patients
subepithelial fibrosis
deposition of types III and V collagen
Mech for basement membrane thickening in asthmatic patients
subepithelial fibrosis
deposition of types III and V collagen
How epithelial damage may contribute to AHR
1) loss of its barrier function to allow penetration of allergens;
2) loss of enzymes (such as neutral endopeptidase) that degrade certain peptide inflammatory mediators;
3) loss of a relaxant factor (so called epithelial-derived relaxant factor);
4) exposure of sensory nerves
How epithelial damage may contribute to AHR
1) loss of its barrier function to allow penetration of allergens;
2) loss of enzymes (such as neutral endopeptidase) that degrade certain peptide inflammatory mediators;
3) loss of a relaxant factor (so called epithelial-derived relaxant factor);
4) exposure of sensory nerves
- Mechanism involved in exercise induced asthma
hyperventilation
results in increased osmolality in airway lining fluid –> triggers mast cell mediator release –>
bronchoconstriction
- Mechanism involved in exercise induced asthma
hyperventilation
results in increased osmolality in airway lining fluid –> triggers mast cell mediator release –>
bronchoconstriction
induce mucus hypersecretion in experimental models of asthma
IL-4
IL-13
mechanism premenstrual worsening of asthma
fall in progesterone
mechanism premenstrual worsening of asthma
fall in progesterone
Mechanism of Exercise-induced asthma (EIA)
prior administration of B2-agonists and antileukotrienes
regular treatment with ICS
Mechanism of Exercise-induced asthma (EIA)
> prior administration of B2-agonists and antileukotrienes
> regular treatment with ICS
may trigger asthma through the release of sulfur dioxide gas in the stomach
Metabisulfite (food preservative)
Increased ambient levels of ____ are associated with increased asthma symptoms
sulfur dioxide, ozone, and nitrogen oxides
reversible occupational asthma
If removed from exposure within the first 6 months of symptoms