Induction of Siglec-F^hiCD101^hi eosinophils in the lungs following murine hookworm Nippostrongylus brasiliensis 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-F^hiCD101^hi, 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 Nippostrongylus brasiliensis (Nb) results in a long-term expansion of distinct Siglec-F^hiCD101^hi eosinophil subpopulations. Nb-elevated eosinophil populations in the bone marrow and circulation did not present this phenotype. Siglec-F^hiCD101^hi 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-F^hiCD101^hi eosinophils. This data identifies a morphologically distinct and persistent subset of Siglec-F^hiCD101^hi lung eosinophils induced following Nb infection. These eosinophils may contribute to long-term pathology following helminth infection.