Background: Although airway angiogenesis and edema have
been proposed to contribute to the airway remodeling process in
patients with asthma, there are few studies looking at these structural
components in the airway tissue of asthma patients. Mycoplasma
infection may be associated with chronic asthma and has been shown to
induce angiogenesis and edema in a murine model.
Participants and measurements: We evaluated blood vessels
and edema by immunohistochemistry in endobronchial biopsy samples from
10 normal control subjects and 15 patients with mild-to-moderate asthma
before and after a 6-week treatment with clarithromycin (n = 8) or
placebo (n = 7). Type IV collagen and α2-macroglobulin
were used to identify blood vessels and edema in the tissue,
respectively. Mycoplasma pneumoniae was evaluated by
polymerase chain reaction.
Setting: National Jewish
Medical and Research Center.
Results: At baseline, the
vascularity, the number of blood vessels, and the edematous area in the
airway tissue were not significantly different between asthmatic
patients and normal control subjects. However, asthmatic patients
demonstrated increased blood vessel size compared with normal control
subjects (p = 0.03). After clarithromycin treatment in asthmatic
patients, the number of blood vessels was increased (p = 0.02), while
edema decreased (p = 0.049). Asthmatic patients who tested positive
for M pneumoniae showed a significant increase in
vascularity than asthmatic patients who tested negative for M
pneumoniae (p = 0.02).
Conclusion: Our data
suggest that angiogenesis and edema may not be significant features of
airway remodeling in patients with chronic, mild-to-moderate asthma.
Clarithromycin treatment in asthmatic patients could reduce the
edematous area as identified by α2-macroglobulin
staining, which may lead to airway tissue shrinkage and cause an
artificial increase in the number of blood vessels.