Identification of a Specific Granular Marker of Zebrafish Eosinophils Enables Development of New Tools for Their Study.

Eosinophils control many aspects of the vertebrate innate immune response. They contribute to homeostasis, inflammatory conditions and defense against pathogens. With the varied functions of eosinophils, they have been found to play both protective and pathogenic roles in many diseases.

In the Thick of It: Formation of the Tuberculous Granuloma and Its Effects on Host and Therapeutic Responses.

The defining pathology of tuberculosis is the granuloma, an organized structure derived from host immune cells that surrounds infecting . As the location of much of the bacteria in the infected host, the granuloma is a central point of interaction between the host and the infecting bacterium. This review describes the signals and cellular reprogramming that drive granuloma formation.

In vivo fluorescence lifetime imaging of macrophage intracellular metabolism during wound responses in zebrafish.

The function of macrophages in vitro is linked to their metabolic rewiring. However, macrophage metabolism remains poorly characterized in situ. Here, we used two-photon intensity and lifetime imaging of autofluorescent metabolic coenzymes, nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) and flavin adenine dinucleotide (FAD), to assess the metabolism of macrophages in the wound microenvironment.

A non-canonical type 2 immune response coordinates tuberculous granuloma formation and epithelialization.

The central pathogen-immune interface in tuberculosis is the granuloma, a complex host immune structure that dictates infection trajectory and physiology. Granuloma macrophages undergo a dramatic transition in which entire epithelial modules are induced and define granuloma architecture. In tuberculosis, relatively little is known about the host signals that trigger this transition.