{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T23:11:11Z","timestamp":1791155471573,"version":"4.1.0"},"reference-count":38,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2009,2,1]],"date-time":"2009-02-01T00:00:00Z","timestamp":1233446400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Immune responses elicited by parasitic worms share many features with those of chronic allergy. Eosinophils contribute to the inflammation that occurs in both types of disease, and helminths can be damaged or killed by toxic products released by eosinophils in vitro. Such observations inform the widely held view that eosinophils protect the host against parasitic worms. The mouse is a natural host for Trichinella spiralis, a worm that establishes chronic infection in skeletal muscle. We tested the influence of eosinophils on T. spiralis infection in two mouse strains in which the eosinophil lineage is ablated. Eosinophils were prominent in infiltrates surrounding infected muscle cells of wild-type mice; however, in the absence of eosinophils T. spiralis muscle larvae died in large numbers. Parasite death correlated with enhanced IFN-\u03b3 and decreased IL-4 production. Larval survival improved when mice were treated with inhibitors of inducible NO synthase, implicating the NO pathway in parasite clearance. Thus, the long-standing paradigm of eosinophil toxicity in nematode infection requires reevaluation, as our results suggest that eosinophils may influence the immune response in a manner that would sustain chronic infection and insure worm survival in the host population. Such a mechanism may be deployed by other parasitic worms that depend upon chronic infection for survival.<\/jats:p>","DOI":"10.4049\/jimmunol.182.3.1577","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:01:40Z","timestamp":1397847700000},"page":"1577-1583","source":"Crossref","is-referenced-by-count":145,"title":["Eosinophil Deficiency Compromises Parasite Survival in Chronic Nematode Infection"],"prefix":"10.1093","volume":"182","author":[{"given":"Valeria","family":"Fabre","sequence":"first","affiliation":[{"name":"James A. Baker Institute for Animal Health, Cornell University , Ithaca, NY 14853"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel P","family":"Beiting","sequence":"additional","affiliation":[{"name":"James A. Baker Institute for Animal Health, Cornell University , Ithaca, NY 14853"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan K","family":"Bliss","sequence":"additional","affiliation":[{"name":"James A. Baker Institute for Animal Health, Cornell University , Ithaca, NY 14853"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nebiat G","family":"Gebreselassie","sequence":"additional","affiliation":[{"name":"James A. Baker Institute for Animal Health, Cornell University , Ithaca, NY 14853"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucille F","family":"Gagliardo","sequence":"additional","affiliation":[{"name":"James A. Baker Institute for Animal Health, Cornell University , Ithaca, NY 14853"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nancy A","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Hematology and Oncology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James J","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona , Scottsdale, AZ 85259"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Judith A","family":"Appleton","sequence":"additional","affiliation":[{"name":"James A. Baker Institute for Animal Health, Cornell University , Ithaca, NY 14853"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2009,2,1]]},"reference":[{"key":"2026012806214714700_R1","first-page":"147","article-title":"The eosinophil.","volume-title":"Annu. Rev. 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Parasitol.","year":"1975"},{"key":"2026012806214714700_R15","first-page":"7","article-title":"Fine structure of the muscle phase of Trichinella spiralis in the mouse. C. Kim, ed.","volume-title":"Trichinellosis","year":"1974"},{"key":"2026012806214714700_R16","first-page":"3129","article-title":"Interleukin-10 limits local and body cavity inflammation during infection with muscle-stage Trichinella spiralis.","volume-title":"Infect. Immun.","year":"2004"},{"key":"2026012806214714700_R17","first-page":"487","article-title":"Interleukin-5 deficient mice exhibit impaired host defence against challenge Trichinella spiralis infections.","volume-title":"Parasite Immunol.","year":"2000"},{"key":"2026012806214714700_R18","first-page":"1387","article-title":"Targeted deletion of a high-affinity GATA-binding site in the GATA-1 promoter leads to selective loss of the eosinophil lineage in vivo.","volume-title":"J. Exp. 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