1. Myelopoiesis in the omentum of normal mice and during abdominal inflammatory processes.
- Author
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Pinho Mde F, Hurtado SP, El-Cheikh MC, Rossi MI, Dutra HS, and Borojevic R
- Subjects
- Animals, Cell Differentiation, Cells, Cultured, Erythroid Precursor Cells immunology, Inflammation pathology, Inflammation physiopathology, Mice, Mice, Inbred C3H, Myeloid Cells metabolism, Omentum anatomy & histology, Omentum pathology, Schistosomiasis mansoni pathology, Schistosomiasis mansoni physiopathology, Abdomen, Leukopoiesis, Omentum physiology, Omentum physiopathology
- Abstract
Coelomic cavities are relatively isolated from the systemic circulation of blood cells. Resident cell populations have a proper phenotype and kinetics, maintaining their steady-state populations and their responsiveness to local inflammatory reactions, in which the number and quality of coelomic cells can be greatly increased and modified. We have addressed the question of whether the increase in cell infiltrate in the inflamed abdominal cavity is sustained by the proliferation of myeloid cells in the omentum, and if so what are the characteristics of the progenitor cells involved and how the omentum controls their proliferation and differentiation. In the omentum under normal conditions and with inflammation due to schistosomal infection we found that pluripotent early myeloid progenitors were capable of giving rise to all the myeloid lineages in clonogenic assays, but not to the totipotent blood stem cells. Besides the major haemopoietins (GM-CSF, M-CSF, G-CSF, IL-5), the omentum stroma constitutively expressed SDF-1 alpha, the chemokine which elicits homing of circulating early haemopoietic progenitors. While normal omentum stroma produced LIF, its expression was substituted by SCF in inflamed tissues. In the first situation a slow steady-state renewal of progenitors is potentially favoured, while their intense expansion may be predominant in the latter one. We propose that the increase in cells in the abdominal cavity in inflammatory reactions is due to the enhanced input and expansion of early myeloid progenitors sustaining the in situ production of abdominal cell populations, rather than to the input of systemic circulating inflammatory cells.
- Published
- 2002
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