PMID- 9477010
OWN - NLM
STAT- MEDLINE
DCOM- 19980409
LR  - 20230317
IS  - 0940-1334 (Print)
IS  - 0940-1334 (Linking)
VI  - 247
IP  - 6
DP  - 1997
TI  - Neuroleptic treatment increases soluble IL-2 receptors and decreases soluble IL-6 
      receptors in schizophrenia.
PG  - 308-13
AB  - The cytokines interleukin-2 (IL-2) and interleukin-6 (IL-6) increase during 
      immune activation, they are released from activated astrocytes and microglial 
      cells in the central nervous system (CNS), and they are able to enhance the 
      catecholaminergic neurotransmission. This study focused on the soluble receptors 
      of IL-2 and IL-6 (sIL-2R, sIL-6R) as a part of the regulation system of IL-2 and 
      IL-6. We studied serum levels of sIL-2R in 30 schizophrenic patients not under 
      neuroleptic medication during an acute exacerbation of the disease and reexamined 
      these patients under neuroleptic treatment after clinical improvement. The sIL-6R 
      levels of 39 schizophrenic patients were estimated under the same conditions. The 
      results were compared with the levels of sIL-2R and sIL-6R in 42 healthy 
      controls. No difference was found between the schizophrenic patients before 
      neuroleptic treatment and the healthy controls. During neuroleptic treatment, 
      however, there was a significant increase of sIL-2R levels and a significant 
      decrease of the sIL-6R levels between the pre- and post-conditions. In comparison 
      with healthy controls, the treatment group also showed increased sIL-2R levels 
      and decreased sIL-6R levels. These results suggest that treatment with 
      neuroleptics is associated with increased sIL-2R and decreased sIL-6R. Since 
      sIL-2R bind and inactivate IL-2, whereas sIL-6R form an active complex with IL-6, 
      the increase of sIL-2R and the decrease of sIL-6R together may reflect a 
      functional down regulation of these activating cytokines. This suggests that 
      neuroleptic therapy has a differentiated immunomodulatory effect.
FAU - Muller, N
AU  - Muller N
AD  - Psychiatric Hospital, Ludwig Maximilian University, Munich, Germany.
FAU - Empl, M
AU  - Empl M
FAU - Riedel, M
AU  - Riedel M
FAU - Schwarz, M
AU  - Schwarz M
FAU - Ackenheil, M
AU  - Ackenheil M
LA  - eng
PT  - Clinical Trial
PT  - Controlled Clinical Trial
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Eur Arch Psychiatry Clin Neurosci
JT  - European archives of psychiatry and clinical neuroscience
JID - 9103030
RN  - 0 (Antipsychotic Agents)
RN  - 0 (Receptors, Interleukin-2)
RN  - 0 (Receptors, Interleukin-6)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Antipsychotic Agents/*adverse effects/therapeutic use
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Receptors, Interleukin-2/*biosynthesis
MH  - Receptors, Interleukin-6/*biosynthesis
MH  - Schizophrenia/drug therapy/*metabolism
MH  - Smoking/metabolism
EDAT- 1997/01/01 00:00
MHDA- 1998/02/26 00:01
CRDT- 1997/01/01 00:00
PHST- 1997/01/01 00:00 [pubmed]
PHST- 1998/02/26 00:01 [medline]
PHST- 1997/01/01 00:00 [entrez]
AID - 10.1007/BF02922260 [doi]
PST - ppublish
SO  - Eur Arch Psychiatry Clin Neurosci. 1997;247(6):308-13. doi: 10.1007/BF02922260.