Am. J. Respir. Crit. Care Med., Vol 151, No. 3, Mar 1995, 873-878.
Toxocara-induced eosinophilic inflammation. Airway function and effect of anti-IL-5
J Buijs, MW Egbers, WH Lokhorst, HF Savelkoul and FP Nijkamp
Department of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, University of Utrecht, The Netherlands.
The immunoinflammatory response to parasitic nematode infections and
allergic diseases have some similarities, the most profound being the
increases in eosinophils and serum total IgE concentration. Whether
parasitic infections stimulate or inhibit allergic asthma is a matter of
debate. We investigated the effect of Toxocara canis (T. canis) infection
on airway function in BALB/c mice at various days post- infection. Within
24 h after infection, the trachea responded hyperreactive to carbachol
stimulation. Eosinophils, and to a lesser degree lymphocytes, infiltrated
the airways causing interstitial and alveolar inflammation (7 d
post-infection). Concurrently with cell infiltration, the trachea became
hyporesponsive to carbachol whereas the pulmonary resistance was increased
and the dynamic compliance decreased. The hyporeactive response could be
simulated in vitro by incubating normal tracheae with eosinophil-enriched
bronchoalveolar lavage cells obtained from infected mice. The response
depended on the number of cells added to the medium, a lower number causing
a hyper- and a higher number a hyporeactive response. Anti-interleukin-5
(anti- IL-5) producing hybridoma cells given simultaneously with T. canis
infection inhibited eosinophil infiltration in the airways but not that of
lymphocytes. Anti-IL-5 treatment prevented tracheal hyporeactivity but not
perivascular and peribronchial edema, increased pulmonary resistance, or
decreased dynamic compliance. Treatment with isotype control antibody did
not affect eosinophil number nor the observed changes in airway functions.
It was concluded that T. canis-induced airway inflammation coincided with
increased pulmonary resistance, decreased dynamic compliance, and
perivascular/peribronchial edema. These phenomena were independent on the
presence of eosinophils, whereas tracheal hyporeactivity was clearly
associated with airway eosinophilia.
