Effects of experimental panic on neuroimmunological functioning.
OBJECTIVE
Psychoimmunological research in panic disorder (PD) so far focussed on single time point evaluation in resting conditions. No robust evidence for changes in the immune system was found using this method. However, PD is characterized by the occurrence of unexpected panic attacks (PAs). The current research focuses on cytokine and acute phase protein (APP) levels and mitogen-induced cytokine secretion following 35% CO(2) inhalation-induced panic.


METHODS
Eighteen PD patients and 18 matched healthy control subjects underwent both a placebo and a 35% CO(2) inhalation on separate days. Blood samples for cytokine and APP determination were taken before and after the inhalation. In addition to serum determination, whole blood samples were cultured and stimulated with mitogens for assessment of the functional capacity of the immune system.


RESULTS
The 35% CO(2) inhalation induced significantly higher levels of anxiety in PD patients as compared to the control subjects, but no differences in immune parameters were found, either in basal conditions or after experimental panic induction.


CONCLUSIONS
In our sample we do not find any changes in serum levels or functional capacity of several immunological parameters in the experimentally provoked PAs. Similar results have been found in social phobia, whereas in other affective disorders such as depression and posttraumatic stress disorder, immune changes are evident. Changes seem to coincide with alterations in hypothalamic-pituitary-adrenal (HPA) axis function. Therefore, the bidirectional communication pathway between the immune system and the HPA axis might play a role in some affective disorders, but it does not specifically seem to be involved in the etiology of PD.
van Duinen
Marlies A
MA
School of Mental Health and Neurosciences, Maastricht University, The Netherlands. marlies.vanduinen@pn.unimaas.nl
Schruers
Koen R J
KR
Kenis
Gunter R L
GR
Wauters
Annick
A
Delanghe
Joris
J
Griez
Eric J L
EJ
Maes
Michael H J
MH
D000209:Acute-Phase Proteins / Q000276:immunology / Q000378:metabolism; D000280:Administration, Inhalation; D000328:Adult; D002245:Carbon Dioxide / Q000008:administration & dosage / Q000009:adverse effects*; D005260:Female; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000276:immunology / Q000378:metabolism; D053590:Interleukin 1 Receptor Antagonist Protein / Q000276:immunology* / Q000378:metabolism; D007376:Interleukin-2 / Q000276:immunology* / Q000378:metabolism; D015850:Interleukin-6 / Q000276:immunology* / Q000378:metabolism; D008297:Male; D016584:Panic Disorder / Q000139:chemically induced / Q000276:immunology / Q000523:psychology; D010913:Pituitary-Adrenal System / Q000276:immunology / Q000378:metabolism
D000209:Acute-Phase Proteins; D053590:Interleukin 1 Receptor Antagonist Protein; D007376:Interleukin-2; D015850:Interleukin-6; D002245:Carbon Dioxide