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Although both malaria and many helminth species use the lungs as a site of development, little attention has been paid to the impact that pulmonary immunity induced by one parasite has on the lung response to the other. To model the consequences of a prior hookworm exposure on the development of immunity to malaria in the lungs, mice were infected with <jats:italic>Nippostrongylus brasiliensis<\/jats:italic> and 2\u00a0weeks later challenged with <jats:italic>Plasmodium berghei<\/jats:italic>. We found that a pre\u2010existing hookworm\u2010induced type 2 immune environment had a measurable but modest impact on the nature of the malaria\u2010driven type 1 cytokine response in the lungs that was associated with a transient effect on parasite development and no significant changes in morbidity and mortality after malaria infection. However, prior hookworm infection did have a lasting effect on lung macrophages, where the malaria\u2010induced M1\u2010like response was blunted by previous M2 polarization. These results demonstrate that, although helminth parasites confer robust changes to the immunological status of the pulmonary microenvironment, lung immunity is plastic and capable of rapidly adapting to consecutive heterologous infections.<\/jats:p>","DOI":"10.1111\/pim.12441","type":"journal-article","created":{"date-parts":[[2017,5,5]],"date-time":"2017-05-05T13:16:46Z","timestamp":1493990206000},"source":"Crossref","is-referenced-by-count":14,"title":["Antecedent <i>Nippostrongylus<\/i> infection alters the lung immune response to <i>Plasmodium berghei<\/i>"],"prefix":"10.1111","volume":"39","author":[{"given":"J. M.","family":"Craig","sequence":"first","affiliation":[{"name":"W. 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