Hematopoiesis is a complex process through which immature bone marrow precursor cells mature into all types of blood cells. Although the association of hematopoietic lineage bias (including anemia and neutrophilia) with chronic inflammatory diseases has long been appreciated, the causes involved are obscure. Recently, cytosolic multiprotein inflammasome complexes were shown to activate inflammatory and immune responses, and directly regulate hematopoiesis in zebrafish models; this was deemed to occur via cleavage and inactivation of the master erythroid transcription factor GATA1. Herein summarized are the zebrafish models that are currently available to study this unappreciated role of inflammasome-mediated regulation of hematopoiesis. Novel putative therapeutic strategies, for the treatment of hematopoietic alterations associated with chronic inflammatory diseases in humans, are also proposed.

造血是一个复杂的过程，未成熟的骨髓前体细胞通过该过程成熟成所有类型的血细胞。尽管人们长期以来都认识到造血谱系偏倚（包括贫血和中性粒细胞减少）与慢性炎症性疾病的关系，但所涉及的原因尚不清楚。最近，在斑马鱼模型中，显示出胞质多蛋白炎性体复合物可激活炎症和免疫反应，并直接调节造血功能。认为这是通过红系主转录因子GATA1的裂解和失活而发生的。本文总结了斑马鱼模型，目前可用于研究炎症小体介导的造血调节的这种未意识到的作用。新的推定治疗策略，