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Reduced thymocyte proliferation but not increased apoptosis as a possible cause of thymus atrophy in iron-deficient mice

Published online by Cambridge University Press:  09 March 2007

Solo R. Kuvibidila ,
Connie Porretta ,
B. Surendra Baliga  and
Lily E. Leiva
Solo R. Kuvibidila*
Affiliation:
Department of Pediatrics, Divisions of Hematology/Oncology and Allergy/Immunology, Louisiana State University Health Sciences Center, 1542 Tulane Avenue, New Orleans LA 70112, USA
Connie Porretta
Affiliation:
Department of Pulmonary Medicine, Louisiana State University, Health Sciences Center, 1542 Tulane Avenue, New Orleans LA 70112, USA
B. Surendra Baliga
Affiliation:
Department of Pediatrics, University of South Alabama College of Medicine, 2451 Fillingim Street, Mobile AL 36617, USA
Lily E. Leiva
Affiliation:
Department of Pediatrics, Divisions of Hematology/Oncology and Allergy/Immunology, Louisiana State University Health Sciences Center, 1542 Tulane Avenue, New Orleans LA 70112, USA
*
*Corresponding author: Dr S. R. Kuvibidila, fax +1 504 568 3078, email [email protected]
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Abstract

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Iron deficiency induces thymus atrophy in laboratory animals and very likely in humans by unknown mechanisms. The atrophy is associated with impaired cell-mediated immunity. In this study, we tested the hypothesis that thymus atrophy is a result of increased apoptosis and reduced thymocyte proliferation. Thymocytes were obtained from twenty-seven control, twenty-seven pairfed, twenty-seven iron-deficient (ID) mice; twelve and fourteen ID mice that received the control diet (0·9 mmol/kg versus 0·09 mmol/kg for the ID diet) for 1 d (repletion, R1) and 3 d (R3), respectively. Cell cycle analysis and apoptosis were studied by flow cytometry using propidium iodide staining and terminal deoxyuridine nick end labeling of DNA breaks assay respectively. When mice were killed, haemoglobin, haematocrit, and liver iron stores of ID, R1, and R3 mice were 25–40 % of those of control and pairfed mice (P<0·01). Absolute and relative thymus weights and thymocyte numbers were 19 to 68 % lower in ID, R1, and R3 than in control and pairfed groups (P<0·05). We found no significant difference among groups in the percentage of cells undergoing apoptosis. A higher percentage of thymocytes from ID and R1 mice than those of control, pairfed, and R3 mice were in the resting phase of the normal cell cycle (P<0·05). Conversely, a lower percentage of thymocytes from ID and R1 mice than those from control, pairfed, and R3 mice were in the DNA synthesis phase and late phase of DNA synthesis and onset of mitosis (G2-M) (P<0·05). Indicators of iron status positively correlated (r 0·3 to 0·56) with the percentage of thymocytes in the G2-M phase (P<0·05). Results suggest that reduced cell proliferation but not increased apoptosis is the cause of thymus atrophy associated with iron deficiency.

Keywords

Iron deficiencyHaemoglobinThymus atrophyCell cycle analysis
Type
Research Article
Information
British Journal of Nutrition , Volume 86 , Issue 2 , August 2001 , pp. 157 - 162
Copyright
Copyright © The Nutrition Society 2001

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