Schubert, Thomas E. O. and Echtenacher, Bernd and Hofstaedter, Ferdinand and Maennel, Daniela N. (2005) Failure of interferon-gamma and tumor necrosis factor in mediating anemia of chronic disease in a mouse model of protracted septic peritonitis. INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 16 (4). pp. 753-758. ISSN 1107-3756,
Full text not available from this repository. (Request a copy)Abstract
Interferon-gamma (IFN-gamma) is considered one of the main inflammatory cytokines contributing to the generation of anemia of chronic disease (ACD). In this study, we used a previously described murine model for ACD based on sublethal cecal ligation and puncture (CLP) with ensuing protracted peritonitis. Within 2 weeks after CLP, a moderate normochromic anemia with low serum iron concentration and preserved iron stores develops, which is consistent with ACD. In order to determine whether IFN-gamma contributes to the development of ACD in vivo, we neutralized IFN-gamma after CLP shortly before and during the phase of most severe bone marrow depression in order to prevent anemia. Additionally, we studied IFN-gamma receptor-deficient mice that underwent CLP. Two weeks after CLP, we determined the red blood cell count, hemoglobin concentration, hematocrit, serum iron concentration, and iron stores in spleens of wild-type mice, IFN-gamma receptor-deficient mice, and mice after neutralization of IFN-gamma. Neutralization of IFN-gamma after CLP could not prevent mice from becoming anemic. Accordingly, IFN-gamma receptor-deficient mice developed anemia to the same extent as wildtype mice. Serum iron concentration was lowered both in IFN-gamma receptor-deficient and wild-type mice. Iron stores in untreated IFN-gamma receptor-deficient mice were elevated compared to untreated wild-type mice. After CLP both IFN-gamma receptor-deficient and wild-type mice had equally overloaded iron stores. Additional neutralization of TNF in IFN-gamma receptor-deficient mice also did not attenuate CLP-induced anemia. Our results clearly demonstrate that neither IFN-gamma alone nor in combination with TNF is a mediator of ACD in our model with transient anemia induced by protracted septic peritonitis.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | COLONY-FORMING-UNITS; TRANSFERRIN RECEPTOR EXPRESSION; PUNCTURE INCREASES MORTALITY; ACUTE-PHASE RESPONSE; IRON-METABOLISM; CECAL LIGATION; INHIBITION; HYPOFERREMIA; MODULATION; MICE; anemia of chronic disease; blood; interferon-gamma; tumor necrosis factor; mouse; septic peritonitis |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Immunologie Medicine > Lehrstuhl für Pathologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 26 Apr 2021 09:14 |
| Last Modified: | 26 Apr 2021 09:14 |
| URI: | https://pred.uni-regensburg.de/id/eprint/35583 |
Actions (login required)
 |
View Item |
