Am. J. Respir. Cell Mol. Biol., Vol 17, No. 2, 08 1997, 203-208.
Acute and long-term effects of stressors on pulmonary immune functions
JH Persoons, NM Moes, E Broug-Holub, K Schornagel, FJ Tilders and G Kraal
Department of Cell Biology and Immunology, Vrije Universiteit, Amsterdam, The Netherlands.
To study the effects of different types or intensities of stressors on
immune reactivity in the lungs, we studied the ex vivo production of nitric
oxide (NO) and IL-1beta by alveolar macrophages (AM) after short exposure
of rats to restraint stress or inescapable electric footshocks. Exposure to
electric footshocks of various intensities resulted in an
intensity-dependent decrease in NO production whereas the IL-1beta
production by AM had increased. The secretory activity was similarly
affected by restraint stress. When the time course of electric footshocks
on secretory functions of AM was studied, it was found that the effects on
NO and IL-1beta production by AM were normalized 3 days after the stress
induction, but reappeared when cells were isolated 1 to 2 wk after stress
exposure. Analysis of the effects of electric footshocks of various
intensities on antibody production 10 days after the stress session and
subsequent lung immunization with trinitrophenyl conjugated keyhole limpet
hemocyanin (TNP-KLH), showed a footshock intensity-dependent response.
Although exposure to stress induced an increase in plasma levels of
adrenocorticotropic hormone (ACTH) and corticosterone (CORT), hormone
levels did not differ between the various stress-exposed groups. This
suggests that the observed stress effects on pulmonary immune functions
were not mediated by ACTH or CORT but point to a direct involvement of the
autonomic nervous system.
