Gene Technology Center


タイトル; Innate immune signaling regulates early hematopoiesis upon acute inflammatory bowel disease.
発表者;林 慶和氏
(熊本大学 国際先端医学研究機構 滝澤研究室)
Hematopoietic stem cells (HSCs) slowly self-renew and differentiate in adult bone marrow (BM), while highly proliferating hematopoietic progenitor cells presumably contribute to daily hematopoiesis. HSCs can be activated to self-renew or differentiate when hematopoietic need is enhanced upon hematopoietic challenges such as inflammation. However, it remains unclear how HSC and progenitors (HSPCs) integrate the demand signal to hematopoietic production in BM and what the biological consequence of HSPC activation is on their fate decision.
We have previously shown that systemic injection of gram-negative bacteria or its component activates dormant HSCs to proliferation through direct activation of Toll like receptor (TLR) 4 signaling, and impairs HSC function (Takizawa et al., Cell Stem Cell 2017). To extend these findings to other inflammatory context, we here study the impact of gut microbiota infiltrated upon gut inflammation on early hematopoiesis by employing inflammatory bowel disease (IBD) model. Acute IBD expanded HSPCs in primary BM and directed their migration to inflamed lymph nodes, suggesting that BM hematopoiesis can sense inflammation occurring in the distal organs and modulates cell proliferation and localization.
Uncovering the underlying mechanism will help to understand inflammatory feedback signals through cross-organ communications that orchestrate hematopoiesis and might be relevant to ageing-
associated chronic disorders.


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