Background Immunological and functional bronchopulmonary abnormalities may
be present in up to two-thirds of patients with Crohn's disease. Having rec
ently described a mild increase in methacholine airways responsiveness in t
hese patients, we investigated whether this physiological abnormality is as
sociated with bronchial inflammation since it has previously been described
in asthma.
Methods Eighteen patients with Crohn's disease and 15 healthy controls matc
hed for age, atopy and smoking habit, were studied. All the subjects underw
ent a bronchial methacholine challenge (1, 4 and 16 mg/mL) and a sputum ind
uction by inhalation of hypertonic saline (NaCl 4.5%). The sputum samples w
ere analysed fur their cellular composition as well as for the levels of se
veral mediators and proteins in the fluid phase, including eosinophil catio
nic protein (ECP), myeloperoxydase, albumin, alpha(2)-macroglobulin, interl
eukin-8 (IL-8), IgA and IL-8/immunoglobulin A complexes.
Results When compared to control subjects, patients with Crohn's disease ha
d significantly higher sputum eosinophil counts (14.5% [0-79.9%] vs 0.2% [0
-2.3%]; P < 0.001) and ECP levels (26.2 mu g/L [4- 124.2 mu g/L] vs 9.8 mu
g/L [0-94.2 mu g/L]; P < 0.05). However, patients with Crohn's disease had
no sign of increased plasma exudation as reflected by sputum levels of albu
min and alpha(2)-macroglobulin similar to those seen in control subjects. F
urthermore the sputum levels of IL-8, IgA and IL-8/IgA complexes were not s
ignificantly different between the two groups. The magnitude of the fall in
forced expiratory volume in Is after methacholine inhalation was significa
ntly increased in Crohn's disease patients although it did not correlate wi
th the extent of sputum eosinophilia or with the sputum ECP levels.
Conclusions Crohn's disease patients without any clinical respiratory invol
vement have airway eosinophilia without local increased plasma exudation. H
owever, bronchial eosinophilia in Crohn's disease per sc is not sufficient
to induce clinically significant airway hyperresponsiveness, suggesting tha
t other factors than bronchial eosinophilic infiltration are required for t
he clinical expression of an airway instability.