Induction of Siglec-F(hi)CD101(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(hi)CD101(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(hi)CD101(hi) eosinophil subpopulations. Nb-elevated eosinophil populations in the bone marrow and circulation did not present this phenotype. Siglec-F(hi)CD101(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(hi)CD101(hi) eosinophils. This data identifies a morphologically distinct and persistent subset of Siglec-F(hi)CD101(hi) lung eosinophils induced following Nb infection. These eosinophils may contribute to long-term pathology following helminth infection.