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Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice
Published on: March 10, 2017
Hepcidin is elevated in mice injected with Mycoplasma arthritidis
Curry L Koening1, Hong-Hua Mu, Adam Van Schelt
1Division of Hematology, Department of Internal Medicine, University of Utah, School of Medicine, 30 North 1900 East, Salt Lake City, 84132, Utah, USA. curry.koening@hsc.utah.edu
Journal of Inflammation (London, England)
|November 26, 2009
Summary
Mycoplasma arthritidis infection causes severe arthritis in mice lacking Toll-like receptor 4 (TLR4). Serum hepcidin, an iron regulator, increases independently of TLR4 or IL-6 signaling.
Area of Science:
- Immunology
- Microbiology
- Hematology
Background:
- Mycoplasma arthritidis (M. arthritidis) causes arthritis and produces a superantigen (MAM).
- MAM activates T cells and interacts with Toll-like receptors (TLR) 2 and 4.
- Hepcidin, an iron regulator, is upregulated by TLR4, IL-6, and IL-1.
Purpose of the Study:
- To evaluate serum hepcidin, iron parameters, and inflammatory markers in M. arthritidis-infected mice with differing TLR4 expression.
- To assess arthritis severity and hepcidin transcript levels in the liver and spleen.
Main Methods:
- Comparison of M. arthritidis-injected C3H/HeJ (TLR4-/-) and C3H/HeSnJ (TLR4+/+) mice over 21 days.
- Measurement of serum hepcidin, transferrin saturation, ferritin, IL-6, IL-1beta, and hemoglobin.
- Assessment of arthritis severity and splenic/hepatic hepcidin mRNA expression.
Main Results:
- C3H/HeJ mice exhibited more severe arthritis and higher serum hepcidin levels than C3H/HeSnJ mice.
- Both groups showed increased serum hepcidin within three days, despite C3H/HeJ mice having defective TLR4 and low IL-6.
- C3H/HeJ mice had delayed splenic hepcidin production, increased IL-1beta, but not IL-6, and elevated serum ferritin with decreased transferrin saturation.
Conclusions:
- Serum hepcidin regulation in response to M. arthritidis is not solely dependent on TLR4 or IL-6.
- IL-1beta may play a role in hepcidin upregulation in TLR4-deficient mice.
- M. arthritidis infection impacts iron homeostasis differently based on TLR4 status.
