Induction of Siglec-FCD101 eosinophils in the lungs following murine hookworm infection.

Helminth-induced eosinophils accumulate around the parasite at the site of infection, or in parasite-damaged tissues well after the helminth has left the site. The role of helminth-elicited eosinophils in mediating parasite control is complex. While they may contribute to direct parasite-killing and tissue repair, their involvement in long-term immunopathogenesis is a concern. In allergic Siglec-FCD101, eosinophils are associated with pathology. Research has not shown if equivalent subpopulations of eosinophils are a feature of helminth infection. In this study, we demonstrate that lung migration of rodent hookworm () results in a long-term expansion of distinct Siglec-FCD101 eosinophil subpopulations. -elevated eosinophil populations in the bone marrow and circulation did not present this phenotype. Siglec-FCD101 lung eosinophils exhibited an activated morphology including nuclei hyper-segmentation and cytoplasm degranulation. Recruitment of ST2 ILC2s and not CD4 T cells to the lungs was associated with the expansion of Siglec-FCD101 eosinophils. This data identifies a morphologically distinct and persistent subset of Siglec-FCD101 lung eosinophils induced following infection. These eosinophils may contribute to long-term pathology following helminth infection.