Abstract:
:Inflammation alters hematopoiesis, often by decreasing erythropoiesis and enhancing myeloid output. The mechanisms behind these changes and how the BM stroma contributes to this process are active areas of research. In this study, we examine these questions in the setting of murine Toxoplasma gondii infection. Our data reveal that infection alters early myeloerythroid differentiation, blocking erythroid development beyond the Pre MegE stage, while expanding the GMP population. IL-6 was found to be a critical mediator of these differences, independent of hepcidin-induced iron restriction. Comparing the BM with the spleen showed that the hematopoietic response was driven by the local microenvironment, and BM chimeras demonstrated that radioresistant cells were the relevant source of IL-6 in vivo. Finally, direct ex vivo sorting revealed that VCAM(+)CD146(lo) BM stromal fibroblasts significantly increase IL-6 secretion after infection. These data suggest that BMSCs regulate the hematopoietic changes during inflammation via IL-6.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Chou DB,Sworder B,Bouladoux N,Roy CN,Uchida AM,Grigg M,Robey PG,Belkaid Ydoi
10.1189/jlb.1011527subject
Has Abstractpub_date
2012-07-01 00:00:00pages
123-31issue
1eissn
0741-5400issn
1938-3673pii
jlb.1011527journal_volume
92pub_type
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