PMID- 12776439
OWN - NLM
STAT- MEDLINE
DCOM- 20030916
LR  - 20161020
IS  - 1088-5412 (Print)
IS  - 1088-5412 (Linking)
VI  - 24
IP  - 2
DP  - 2003 Mar-Apr
TI  - Understanding asthma pathophysiology.
PG  - 79-83
AB  - Asthma is best described as a chronic disease that involves inflammation of the 
      pulmonary airways and bronchial hyperresponsiveness that results in the clinical 
      expression of a lower airway obstruction that usually is reversible. 
      Physiologically, bronchial hyperresponsiveness is documented by decreased 
      bronchial airflow after bronchoprovocation with methacholine or histamine. Other 
      triggers that provoke airway obstruction include cold air, exercise, viral upper 
      respiratory infection, cigarette smoke, and respiratory allergens. Bronchial 
      provocation with allergen induces a prompt early phase immunoglobulin E 
      (IgE)-mediated decrease in bronchial airflow (forced expiratory volume in 1 
      second) followed in many patients by a late-phase IgE-mediated reaction with a 
      decrease in bronchial airflow for 4-8 hours. The gross pathology of asthmatic 
      airways displays lung hyperinflation, smooth muscle hypertrophy, lamina 
      reticularis thickening, mucosal edema, epithelial cell sloughing, cilia cell 
      disruption, and mucus gland hypersecretion. Microscopically, asthma is 
      characterized by the presence of increased numbers of eosinophils, neutrophils, 
      lymphocytes, and plasma cells in the bronchial tissues, bronchial secretions, and 
      mucus. Initially, there is recruitment of leukocytes from the bloodstream to the 
      airway by activated CD4 T-lymphocytes. The activated T-lymphocytes also direct 
      the release of inflammatory mediators from eosinophils, mast cells, and 
      lymphocytes. In addition, the subclass 2 helper T-lymphocytes subset of activated 
      T-lymphocytes produces interleukin (IL)-4, IL-5, and IL-13. IL-4 in conjunction 
      with IL-13 signals the switch from IgM to IgE antibodies. The cross-linkage of 
      two IgE molecules by allergen causes mast cells to degranulate, releasing 
      histamine, leukotrienes, and other mediators that perpetuate the airway 
      inflammation. IL-5 activates the recruitment and activation of eosinophils. The 
      activated mast cells and eosinophils also generate their cytokines that help to 
      perpetuate the inflammation. Regardless of the triggers of asthma, the repeated 
      cycles of inflammation in the lungs with injury to the pulmonary tissues followed 
      by repair may produce long-term structural changes ("remodeling") of the airways. 
      This review will discuss in greater detail the relationships of inflammation and 
      airway hyperresponsiveness to the pathophysiology of asthma.
FAU - Fireman, Philip
AU  - Fireman P
AD  - Department of Allergy and Immunology, University of Pittsburgh School of 
      Medicine, Children's Hospital of Pittsburgh, 3705 Fifth Avenue, Pittsburgh, PA 
      15213, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Allergy Asthma Proc
JT  - Allergy and asthma proceedings
JID - 9603640
SB  - IM
MH  - Airway Obstruction/epidemiology/immunology/physiopathology
MH  - Asthma/epidemiology/immunology/*physiopathology
MH  - Bronchial Hyperreactivity/epidemiology/immunology/physiopathology
MH  - Humans
MH  - Prevalence
MH  - Problem-Based Learning
MH  - Risk Factors
RF  - 25
EDAT- 2003/06/05 05:00
MHDA- 2003/09/17 05:00
CRDT- 2003/06/05 05:00
PHST- 2003/06/05 05:00 [pubmed]
PHST- 2003/09/17 05:00 [medline]
PHST- 2003/06/05 05:00 [entrez]
PST - ppublish
SO  - Allergy Asthma Proc. 2003 Mar-Apr;24(2):79-83.