PMID- 18472921
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20120910
LR  - 20211020
IS  - 0962-9351 (Print)
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Linking)
VI  - 3
IP  - 1
DP  - 1994
TI  - Cytokine Detection and Modulation in Acute Graft vs. Host Disease in Mice.
PG  - 33-40
AB  - A murine model for acute lethal graft vs. host disease (GVHD) was used to study 
      the role that a number of cytokines play in the development of lethal GVHD. In 
      this study we focused on the role of IL-1, IL-2, IL-4, IL-6, IFN-gamma and 
      TNF-alpha. Lethally irradiated (C57BL x CBA)F1 mice were reconstituted either 
      with 10(7) allogeneic BALB/c spleen cells or with a similar number of syngeneic 
      cells, as a control. A significant rise in serum levels of IL-6, TNF-alpha and 
      IFN-gamma levels was found in allogeneically reconstituted mice. This is in 
      contrast to the syngeneic control group in which no rise was seen. Serum IL-2 and 
      IL-4 levels were below the detection limit. In the supernatant of Con A 
      stimulated spleen cells from allogeneically reconstituted mice IL-6, IFN-gamma 
      and TNF-alpha concentrations were increased. The expression of mRNA for cytokines 
      as detected by reverse transcription PCR was studied in spleen cells. In the 
      allogeneic reconstituted mice the mRNA expression of IL-1alpha, IL-2, IL-6, 
      IFN-gamma and TNF-alpha displayed faster kinetics compared with that in syngeneic 
      reconstituted mice. The effect of treatment with recombinant cytokines, 
      antibodies to cytokines and to cytokine receptors on the development of GVHD was 
      investigated. Administration of recombinant IL-2 to allogeneically reconstituted 
      mice strongly increased the morbidity and mortality whereas injection of 
      IL-1alpha and TNF-alpha did not influence survival. Administration of antibodies 
      against IL-2 or the IL-2 receptor decreased the morbidity and mortality. 
      Anti-IL-6, anti-IFN-gamma, and anti-TNF-alpha mAB, on the other hand, did not 
      affect the morbidity and mortality of GVHD. The results of this study suggest 
      successive waves of cytokine-secreting cell populations consistent with the 
      induction of an inflammatory response in the development of acute GVH disease.
FAU - Knulst, A C
AU  - Knulst AC
AD  - Department of Immunology Erasmus University Rotterdam The Netherlands.
FAU - Tibbe, G J
AU  - Tibbe GJ
FAU - Bril-Bazuin, C
AU  - Bril-Bazuin C
FAU - Breedland, E G
AU  - Breedland EG
FAU - van Oudenaren, A
AU  - van Oudenaren A
FAU - Benner, R
AU  - Benner R
FAU - Savelkoul, H F
AU  - Savelkoul HF
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
PMC - PMC2367011
EDAT- 1994/01/01 00:00
MHDA- 1994/01/01 00:01
CRDT- 1994/01/01 00:00
PHST- 1993/10/21 00:00 [received]
PHST- 1993/11/17 00:00 [accepted]
PHST- 1994/01/01 00:00 [pubmed]
PHST- 1994/01/01 00:01 [medline]
PHST- 1994/01/01 00:00 [entrez]
AID - S0962935194000062 [pii]
AID - 10.1155/S0962935194000062 [doi]
PST - ppublish
SO  - Mediators Inflamm. 1994;3(1):33-40. doi: 10.1155/S0962935194000062.