PMID- 15720444
OWN - NLM
STAT- MEDLINE
DCOM- 20050412
LR  - 20181113
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 114
IP  - 3
DP  - 2005 Mar
TI  - Exposure to mercuric chloride during the induction phase and after the onset of 
      collagen-induced arthritis enhances immune/autoimmune responses and exacerbates 
      the disease in DBA/1 mice.
PG  - 428-37
AB  - In susceptible mice, mercuric chloride induces a systemic autoimmune response 
      that is characterized by elevated serum levels of immunoglobulin G1 (IgG1) and 
      immunoglobulin E (IgE), production of anti-nucleolar antibodies (ANolAs) and the 
      formation of renal IgG deposits. We have previously shown that mercury can also 
      enhance immune/autoimmune responses in mouse strains genetically prone to develop 
      spontaneous autoimmune disease. Here, we investigated whether mercury can enhance 
      the severity of murine collagen-induced arthritis (CIA), an inducible (acquired) 
      autoimmune disease that cannot be induced by mercury itself. While mercury 
      administered prior to the induction phase of CIA exerted little, if any, 
      influence, administration of mercury during the induction phase and following 
      onset aggravated the symptoms of this disease and increased the serum levels of 
      IgE and IgG2a antibodies directed against collagen type II (CII). Furthermore, 
      while animals injected with mercury alone exhibited a significant decrease in the 
      ratio of the levels of interferon-gamma (IFN-gamma) to interleukin-4 (IL-4) mRNA 
      in their spleens, this ratio was increased in mice with CIA, with or without 
      administration of mercury. Finally, the production of anti-nuclear antibodies, a 
      hallmark of autoimmunity in response to mercury, was observed in all mice with 
      CIA treated with this heavy metal. Our findings suggest that exposure to mercury 
      during the development of CIA may influence immunological factors in such a way 
      as to synergistically promote disease development.
FAU - Hansson, Monika
AU  - Hansson M
AD  - Department of Immunology, the Wenner-Gren Institute, Arrhenius Laboratories for 
      the Natural Sciences, Stockholm University, Stockholm, Sweden.
FAU - Djerbi, Mounira
AU  - Djerbi M
FAU - Rabbani, Hodjattallah
AU  - Rabbani H
FAU - Mellstedt, Hakan
AU  - Mellstedt H
FAU - Gharibdoost, Farhad
AU  - Gharibdoost F
FAU - Hassan, Moustapha
AU  - Hassan M
FAU - Depierre, Joseph W
AU  - Depierre JW
FAU - Abedi-Valugerdi, Manuchehr
AU  - Abedi-Valugerdi M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Antibodies, Antinuclear)
RN  - 0 (Collagen Type II)
RN  - 0 (Immunoglobulin G)
RN  - 0 (RNA, Messenger)
RN  - 207137-56-2 (Interleukin-4)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 53GH7MZT1R (Mercuric Chloride)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Antibodies, Antinuclear/biosynthesis
MH  - Arthritis, Experimental/*chemically induced/immunology/pathology
MH  - Autoimmune Diseases/*chemically induced/immunology/pathology
MH  - Collagen Type II/immunology
MH  - Female
MH  - Gene Expression Regulation/drug effects
MH  - Immunoglobulin E/biosynthesis
MH  - Immunoglobulin G/biosynthesis
MH  - Interferon-gamma/biosynthesis/genetics
MH  - Interleukin-4/biosynthesis/genetics
MH  - Mercuric Chloride/immunology/*toxicity
MH  - Mice
MH  - Mice, Inbred DBA
MH  - RNA, Messenger/genetics
MH  - Spleen/immunology
PMC - PMC1782090
EDAT- 2005/02/22 09:00
MHDA- 2005/04/13 09:00
PMCR- 2006/03/01
CRDT- 2005/02/22 09:00
PHST- 2005/02/22 09:00 [pubmed]
PHST- 2005/04/13 09:00 [medline]
PHST- 2005/02/22 09:00 [entrez]
PHST- 2006/03/01 00:00 [pmc-release]
AID - IMM2105 [pii]
AID - 10.1111/j.1365-2567.2005.02105.x [doi]
PST - ppublish
SO  - Immunology. 2005 Mar;114(3):428-37. doi: 10.1111/j.1365-2567.2005.02105.x.