In
status asthmaticus (SA), severe bronchial
inflammation is associated with acute
respiratory failure. Neutrophils are the prominent cells found in bronchi from SA patients, but eosinophils are also recruited within the first 48 h after the beginning of
mechanical ventilation (MV).
Interleukin (IL)-5 and
CC chemokines have been directly implicated in the pathophysiology of allergic
asthma. However, their involvement in SA had not been determined. The aim of this study was to evaluate the production of
CC chemokines and of
IL-5 in airways from ventilated patients with SA as compared with mild
asthma (A), and to assess the role of these mediators in eosinophil recruitment. We measured levels of the
chemokines monocyte chemotactic proteins (MCPs)-1 and -3; regulated on activation, normal T-cell expressed and secreted (
RANTES); macrophage inflammatory
peptide (MIP)-1alpha; and eotaxin; and of the
cytokine IL-5 in bronchial lavage fluid (BLF) from 10 SA patients, four patients without respiratory disease but undergoing ventilation (V) who were receiving MV, 11 patients with A, and eight healthy volunteers (C). We further evaluated in vitro eosinophil chemotactic activity of BLF from the various groups. Levels of MCP-1,
MIP-1alpha,
RANTES, and
IL-5 were significantly higher in the SA than in the V, A, and C groups. MCP-3 and eotaxin values were not significantly different in the SA and other groups; however, their levels, as well as those of
MIP-1alpha,
RANTES, and
IL-5 correlated with eosinophil influx. Eosinophil chemotactic activity in BLF was increased in asthmatic subjects (A and SA groups) as compared with the other groups, and in SA patients as compared with A patients. Addition of neutralizing anti-IL-5, anti-MCP-3, anti-eotaxin, and anti-
RANTES antibodies significantly inhibited the eosinophil chemotactic activity as compared with that of native BLF. This study shows that the levels of various
CC chemokines and
IL-5 are increased in airways of SA patients, and are potentially involved in eosinophil recruitment.