The zebrafish has been an extremely successful model organism for the study of hematopoiesis (Bennett et al. 2001; de Jong and Zon 2005; Thisse and Zon 2002). Despite the advances in our understanding of blood cell origins and formation, less is known about how these blood cells participate in innate immunity. In particular, macrophages, neutrophils, and dendritic cells are indispensable to innate immunity in higher vertebrates and presumably play a similar role in zebrafish. While macrophages and neutrophils have been characterized (Bennett et al. 2001; de Jong and Zon 2005; Thisse and Zon 2002), dendritic cells have not.
The importance of phagocytes to zebrafish innate immunity is bolstered by data showing that both adult and embryonic macrophages infected by Mycobacterium marinum phagocytosed the bacteria and formed granuloma-like aggregates during in vivo studies (Davis et al. 2002). Additionally, it was shown that M. marinum infection could disrupt the hematopoietic program, causing early microglia destined for the brain to be redirected. In panther mutants, which lack functional macrophage colony stimulating factor receptor (M-CSF-R), infection did not disrupt macrophage recruitment, indicating that such activity is M-CSF-R-independent (Davis et al. 2002). Further evidence of phagocytic function in zebrafish has been established by our laboratory through an in vivo, fluorescence-based respiratory burst assay designed to detect reactive oxygen species (Hermann et al. 2004). The data showed areas of respiratory burst colocalized with phagocytes, as detected by the uptake of the phagocyte-specific dye neutral red.
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