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Updated: May 1, 2026
The Utilization of Oropharyngeal Intratracheal PAMP Administration and Bronchoalveolar Lavage to Evaluate the Host Immune Response in Mice
Published on: April 3, 2014
Inhaled LPS induces blood release of Clara cell specific protein (CC16) in human beings
Olivier Michel1, Robert Murdoch, Alfred Bernard
1Clinics of Allergology and Respiratory Diseases, Saint-Pierre University Hospital, Free University of Brussels, Rue Haute 322, B-1000 Brussels, Belgium. omichel@ulb.ac.be
Background:
Animal models of lung inflammation have validated the plasma 16-kd Clara cell protein (CC16) as a peripheral marker of the permeability of the alveolocapillary barrier.
Objective:
We investigated in human beings whether inhaled LPS induced a rise in airways permeability measured by the plasma changes in CC16.
Methods:
The CC16 was measured in plasma from 15 subjects exposed to LPS by inhalation, during which the kinetics and the dose-response relationship of LPS-induced CC16 were evaluated. Because LPS-induced response involves macrophages activation, the protective effect of oral methylprednisolone was also evaluated.
Results:
An inhalation of 50 microg LPS induced a significant ( P < .001) rise in CC16 after 6 hours (from 7.24 [+/-0.68] microg/L to 10.69 [+/-0.99] microg/L) that normalized at 24 hours (6.65 [+/-0.33] microg/L). The CC16 response was dose-related, with the no-response threshold 0.5 microg LPS. A 6-day treatment with 20 mg/d methylprednisolone inhibited significantly ( P < .001) the CC16 response to 50 microg LPS.
Conclusion:
Exposure to LPS by inhalation in healthy subjects induces an intravascular leakage of CC16 that can be blocked by corticosteroids. These observations further validate plasma CC16 as a noninvasive test of the alveolocapillary barrier permeability.
