PMID- 10651952
OWN - NLM
STAT- MEDLINE
DCOM- 20000210
LR  - 20190513
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 99
IP  - 1
DP  - 2000 Jan
TI  - The role of endogenous steroid hormones in the generation of T helper 2-mediated 
      autoimmunity in mercuric chloride-treated Brown-Norway rats.
PG  - 141-6
AB  - Injection of Brown-Norway rats with mercuric chloride (HgCl2) activates a T 
      helper type 2 (Th2) autoimmune response, with production of a number of 
      autoantibodies and vasculitis primarily affecting the gut. Glucocorticoids have 
      been shown to suppress Th1 and to promote the development of Th2-type responses. 
      Conversely dehydroepiandrosterone (DHEA) promotes Th1 responses with suppression 
      of Th2 responses. This study set out to define the role of these hormones in this 
      animal model. Rats were adrenalectomized (Adx) with no steroid replacement (n = 
      11), Adx with basal steroid replacement given by a 25 mg corticosterone pellet 
      inserted subcutaneously (n = 13), or sham-Adx (n = 14) prior to administration of 
      HgCl2. In both groups of Adx animals there was a delay in the production of 
      immunoglobulin E (IgE) and serum concentrations on day 9 were marginally lower (P 
      = 0.035, repeated measures ANOVA). All of the animals Adx with no steroid 
      replacement and two Adx animals with steroid replacement died between 10 and 14 
      days after HgCl2 challenge. There was no difference in the severity of caecal 
      vasculitis between the groups. A significant increase in adrenal size was noted 
      following administration of HgCl2. Administration of subcutaneous DHEA implants 
      (100 mg and 200 mg) had no significant effect on IgE concentrations or severity 
      of vasculitis. These observations do not support the hypothesis that 
      corticosterone and DHEA play a central role in setting the Th1/Th2 balance in 
      this experimental Th2-mediated autoimmune disease; in contrast with the 
      Th1-mediated autoimmune disease experimental allergic encephalomyelitis where 
      corticosterone plays a key role in immunoregulation.
FAU - MacPhee, I A
AU  - MacPhee IA
AD  - Departments of *Renal Medicine and Pathology, St. George's Hospital Medical 
      School, Cranmer Terrace, London, UK.
FAU - Turner, D R
AU  - Turner DR
FAU - Oliveira, D B
AU  - Oliveira DB
LA  - eng
PT  - Journal Article
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Glucocorticoids)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 53GH7MZT1R (Mercuric Chloride)
RN  - 57B09Q7FJR (Dehydroepiandrosterone Sulfate)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Adrenal Glands/drug effects/pathology
MH  - Adrenalectomy
MH  - Analysis of Variance
MH  - Animals
MH  - Autoimmunity
MH  - Cecal Diseases/chemically induced/immunology
MH  - Corticosterone/pharmacology
MH  - Dehydroepiandrosterone Sulfate/pharmacology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Glucocorticoids/*pharmacology
MH  - Hypertrophy
MH  - Immunoglobulin E/*blood
MH  - Mercuric Chloride
MH  - Rats
MH  - Rats, Inbred BN
MH  - Th2 Cells/*immunology
MH  - Time Factors
MH  - Vasculitis/chemically induced/immunology
PMC - PMC2327119
EDAT- 2000/01/29 00:00
MHDA- 2000/01/29 00:01
PMCR- 2001/01/01
CRDT- 2000/01/29 00:00
PHST- 2000/01/29 00:00 [pubmed]
PHST- 2000/01/29 00:01 [medline]
PHST- 2000/01/29 00:00 [entrez]
PHST- 2001/01/01 00:00 [pmc-release]
AID - imm924 [pii]
AID - 10.1046/j.1365-2567.2000.00924.x [doi]
PST - ppublish
SO  - Immunology. 2000 Jan;99(1):141-6. doi: 10.1046/j.1365-2567.2000.00924.x.