Chronic Trichuris muris infection alters hematopoiesis and causes IFN-γ-expressing T-cell accumulation in the mouse bone marrow

Alistair L. Chenery, Frann Antignano, Michael R. Hughes, Kyle Burrows, Kelly M. McNagny, Colby Zaph

Research output: Contribution to journalArticleResearchpeer-review

8 Citations (Scopus)


Proinflammatory cytokines produced during immune responses to infectious stimuli are well-characterized to have secondary effects on the function of hematopoietic progenitor cells in the BM. However, these effects on the BM are poorly characterized during chronic infection with intestinal helminth parasites. In this study, we use the Trichuris muris model of infection and show that Th1 cell-associated, but not acute Th2 cell-associated, responses to chronic T. muris infection cause a major, transient expansion of CD48CD150 multipotent progenitor cells in the BM that is dependent on the presence of adaptive immune cells and IFN-γ signaling. Chronic T. muris infection also broadly stimulated proliferation of BM progenitor cells including CD48CD150+ hematopoietic stem cells. This shift in progenitor activity during chronic T. muris infection correlated with a functional increase in myeloid colony formation in vitro as well as neutrophilia in the BM and peripheral blood. In parallel, we observed an accumulation of CD4+, CD8+, and CD4CD8 (double negative) T cells that expressed IFN-γ, displaying activated and central memory-type phenotypes in the bone marrow during chronic infection. Thus, these results demonstrate that Th1 cell-driven responses in the intestine during chronic helminth infection potently influence upstream hematopoietic processes in the BM via IFN-γ.
Original languageEnglish
Pages (from-to)2587-2596
Number of pages10
JournalEuropean Journal of Immunology
Issue number11
Publication statusPublished - Nov 2016


  • Bone marrow
  • Hematopoiesis
  • HSC
  • IFN-γ
  • T cells
  • Trichuris muris

Cite this