Infection-Induced Changes in Hematopoiesis

Zaretsky, Arielle Glatman; Engiles, Julie B.; Hunter, Christopher A.

doi:10.4049/jimmunol.1302061

Cited by 81 publications

(76 citation statements)

References 107 publications

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“…Rather, emergency hematopoiesis has been described in a number of infectious events and in response to other TLR agonists. [37][38][39][40][41] One important difference between flagellin and such agonists is that flagellin does not induce large amounts of master proinflammatory cytokines such as tumor necrosis factor a and IL-12 p70, enabling it to be administered repeatedly at doses similar to those used here without significant clinical-type adverse events. Another difference is that some TLR agonists are reported to directly act upon LSK cells, which was not the case in our study.…”

Section: Discussionmentioning

confidence: 99%

TLR5 signaling in murine bone marrow induces hematopoietic progenitor cell proliferation and aids survival from radiation

et al. 2017

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Section: Discussionmentioning

confidence: 99%

TLR5 signaling in murine bone marrow induces hematopoietic progenitor cell proliferation and aids survival from radiation

et al. 2017

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“…1,2 Under conditions of stress, such as injury or infection, hematopoiesis can increase in capacity, to provide the blood cells necessary to promote inflammation, wound healing, and/or the elimination of pathogens. [3][4][5][6][7] Although coordinated alterations in hematopoiesis can be beneficial, dysregulated responses can result in the development of unchecked inflammation and thus contribute to various disease states, including colitis, asthma, and allergies. 6,[8][9][10] Moreover, recent studies have demonstrated that the contributions of hematopoiesis to the development of inflammation are not limited to events occurring in the bone marrow, and that hematopoietic progenitor cells can enter the periphery and traffic directly to sites of inflammation.…”

Section: Introductionmentioning

confidence: 99%

In situ hematopoiesis: a regulator of TH2 cytokine-mediated immunity and inflammation at mucosal surfaces

et al. 2015

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Hematopoiesis refers to the development of blood cells in the body through the differentiation of pluripotent stem cells. Although hematopoiesis is a multifocal process during embryonic development, under homeostatic conditions it occurs exclusively within the bone marrow. There, a limited number of hematopoietic stem cells differentiate into a rapidly proliferating population of lineage-restricted progenitors that serve to replenish circulating blood cells. However, emerging reports now suggest that under inflammatory conditions, alterations in hematopoiesis that occur outside of the bone marrow appear to constitute a conserved mechanism of innate immunity. Moreover, recent reports have identified previously unappreciated pathways that regulate the egress of hematopoietic progenitor cells from the bone marrow, alter their activation status, and skew their developmental potential. These studies suggest that progenitor cells contribute to inflammatory response by undergoing in situ hematopoiesis (ISH). In this review, we highlight the differences between homeostatic hematopoiesis, which occurs in the bone marrow, and ISH, which occurs at mucosal surfaces. Further, we highlight factors produced at local sites of inflammation that regulate hematopoietic progenitor cell responses and the development of TH2 cytokine-mediated inflammation. Finally, we discuss the therapeutic potential of targeting ISH in preventing the development of inflammation at mucosal sites.

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“…When vertebrates are infected by pathogens such as bacteria, the immune cells, particularly mononuclear (monocytes/macrophages) and polymorphonuclear (granulocytes) myeloid phagocytes, respond immediately1. A slight infection such as a localised bacterial challenge induces the recruitment of myeloid phagocytes, particularly granulocytes, from the bloodstream, but exerts a limited influence on their exhaustion and expansion23.…”

mentioning

confidence: 99%

“…Although these physiologically dormant HSCs quickly enter the cell cycle upon challenge456789, how they react to pathogens remains unclear, primarily because of the difficulty in isolating pure HSCs34. However, the response of HSPCs and their subsequent developmental potential under demand-derived emergency conditions, such as when encountering pathogens or when stimulated by cytokines, has been the focus of research recently146. Different pathogens induce different HSPC reactions6.…”

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confidence: 99%

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Systemic inoculation of Escherichia coli causes emergency myelopoiesis in zebrafish larval caudal hematopoietic tissue

Hou

Sheng

Mao

et al. 2016

Sci Rep

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Emergency granulopoiesis occurs in response to severe microbial infection. However, whether and how other blood components, particularly monocytes/macrophages and their progenitors, including hematopoietic stem/progenitor cells (HSPCs), participate in the process and the underlying molecular mechanisms remain unknown. In this study, we challenged zebrafish larvae via direct injection of Escherichia coli into the bloodstream, which resulted in systemic inoculation with this microbe. The reaction of hematopoietic cells, including HSPCs, in the caudal hematopoietic tissue was carefully analysed. Both macrophages and neutrophils clearly expanded following the challenge. Thus, emergency myelopoiesis, including monopoiesis and granulopoiesis, occurred following systemic bacterial infection. The HSPC reaction was dependent on the bacterial burden, manifesting as a slight increase under low burden, but an obvious reduction following the administration of an excessive volume of bacteria. Pu.1 was important for the effective elimination of the microbes to prevent excessive HSPC apoptosis in response to stress. Moreover, Pu.1 played different roles in steady and emergency monopoiesis. Although Pu.1 was essential for normal macrophage development, it played suppressive roles in emergency monopoiesis. Overall, our study established a systemic bacterial infection model that led to emergency myelopoiesis, thereby improving our understanding of the function of Pu.1 in this scenario.

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Infection-Induced Changes in Hematopoiesis

Cited by 81 publications

References 107 publications

TLR5 signaling in murine bone marrow induces hematopoietic progenitor cell proliferation and aids survival from radiation

TLR5 signaling in murine bone marrow induces hematopoietic progenitor cell proliferation and aids survival from radiation

In situ hematopoiesis: a regulator of TH2 cytokine-mediated immunity and inflammation at mucosal surfaces

Systemic inoculation of Escherichia coli causes emergency myelopoiesis in zebrafish larval caudal hematopoietic tissue

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